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AMBULATORY BLOOD PRESSURE BIOSITUATIONAL FEEDBACK
AND SYSTOLIC BLOOD PRESSURE ESTIMATION
SANDRA WOLFE CITY
A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL
OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
DOCTOR OF PHILOSOPHY
UNIVERSITY OF FLORIDA
This dissertation is dedicated to my husband and children,
Jeff, Meghan, and Matthew;
in loving memory of Eric A. Wolfe;
and to my three wonderful families,
the McGrogans, the Wolfes, and the Cittys.
Thank you to Jeff for being a wonderful friend, husband, and father.
Thank you to Meghan and Matthew for being the best little researchers,
data collectors, and children in the world.
Thank you to my mom, Liz, for helping with babysitting and grandma things.
Thank you to my sister, Susan, for her support through this process.
I love you all very much!
Thank you, God!
I gratefully acknowledge the assistance of my dissertation chairperson, Carolyn
Yucha, PhD, for her mentoring, guidance, humor, encouragement, patience, and wisdom
throughout the course of my 4 years at the University of Florida.
I gratefully acknowledge the support of the University of Florida College of
Nursing, UF College of Nursing Office for Research Support, N. Florida/S. Georgia VA
Health System, and Sigma Theta Tau Alpha Theta Chapter International Nursing Honor
Society for partial funding of this project.
I am extremely grateful to Maude Rittman, PhD for her guidance and mentoring
during my Predoctoral Nurse Fellowship at the Gainesville VAMC. I gratefully
acknowledge Ms. Susan Nadeau and the staff at the Brain Rehabilitation Research Center
and Rehabilitation Outcomes Research Center for their assistance with acquiring research
office space and subject recruitment. I also would like to extend my deepest appreciation
to my dissertation committee members-Maude Rittman, PhD, Joyce Stechmiller, PhD,
and Keith Berg, PhD-for their contributions and support of this project.
TABLE OF CONTENTS
ACKNOWLEDGMENTS ................. .......................... iii
ABSTRACT ................ ................................... vi
1 INTRODUCTION .......................................... 1
Definition and Scope of the Problem ................................... 1
Problem Statement ........... ....................................... 7
Purposes of the Study .......................................... 8
Hypotheses ....................................... ............ 9
D efinitions of Term s ................................. ............. 9
Limitations ................. .. .................... ............. 11
Significance of the Study ............... ........................ 11
2 REVIEW OF LITERATURE ................ ..................... 13
Theories of Hypertension Development ............................ 13
Systolic Hypertension ................ .......................... 25
Issues Surrounding the Treatment of Hypertension .......................... 26
Biosituational Factors Associated with High BP ............................ 31
BP Awareness and Estimation ............... ....................... 38
Educational Level and Health Disparities ................................. 49
Ambulatory BP Monitoring ............... ......................... 50
Summary ............... ............................ .52
3 PROCEDURES AND METHODS ..................................... 53
Research Design ................................................... 53
Population and Sample .............. .................... ......... 53
Inclusion and Exclusion Criteria ................ ................... .. 55
Research Variables and Instruments .................................. 56
Study Protocol and Procedures ...................................... 63
Methods of Statistical Analyses .................. .................... 68
4 RESULTS ........................................... ............. 71
Descriptive Results ................. ............................ 71
Analytic Results for Hypotheses .................................... 75
Hypotheses ............ ............................................ 78
5 DISCUSSION AND RECOMMENDATIONS ............................ 93
Discussion of Results .......... ................... ........... 93
Conclusions ......... .... ..................... .... ......... 105
Implications for Clinical Practice ................. ................... 106
Recommendations for Future Research .............................. 108
A PRE-/POSTTRAINING SBP ESTIMATION FORM ...................... 110
B SBP ESTIMATION STUDY TRAINING FORM ....................... 111
C SBP ESTIMATION STUDY TRAINING FORM ....................... 113
D HEALTH HISTORY FORM ......................................... 115
REFERENCES ............. .......................................... 117
BIOGRAPHICAL SKETCH ............................................ 126
Abstract of Dissertation Presented to the Graduate School
of the University of Florida in Partial Fulfillment of the
Requirements for the Degree of Doctor of Philosophy
AMBULATORY BLOOD PRESSURE BIOSITUATIONAL FEEDBACK
AND SYSTOLIC BLOOD PRESSURE ESTIMATION
Sandra Wolfe Citty
Chair: Carolyn Yucha
Major Department: Nursing
In an age of technological advances and medical breakthroughs, hypertension continues
to be a devastating threat throughout the United States and worldwide. From 1987 to
1997, the death rate from high blood pressure increased by 13.1%. Difficulties in
detection and treatment exist because hypertension is a relatively silent disease, for which
patients are often asymptomatic and are feeling well. Because of the lack of observable
symptoms associated with high blood pressure, patients with hypertension often have
difficulty prescribing meaning to their disease threat or treatment requirements. The
primary purpose of this research was to determine if subjects with hypertension can
improve their awareness of their systolic blood pressure after participating in the
ambulatory blood pressure and biosituational self-awareness training intervention. A
repeated measure, pretest/posttest design was used for this study. Thirty-nine adult
hypertensive subjects participated in the study. There were no significant differences
among the group of hypertensives after training compared to before training, using a
paired samples t-test. There were, however significant differences in improvement of
estimating SBP among the subgroup of college-educated hypertensives (p = 0.04) and
between the groups who used and did not use antihypertensive medications (p = 0.05).
Hypertensives who did not take medications showed significant improvement compared
to antihypertensive medication users. This study provides support for using feedback
methods to improve the ability to estimate BP in certain populations, specifically college
educated hypertensives and hypertensives who are not taking antihypertension
medications, and suggests that BP awareness may be improved in selected people using
This chapter introduces concepts that are under investigation including the
significance of hypertension, problems with detection and treatment of high blood
pressure (BP), factors associated with dismal treatment rates, potential manifestations or
factors associated with high BP levels, and estimation of BP. This chapter will describe
the definition and scope of the problem, the main research problem to be investigated,
and the significance of the study. The definition of major terms, assumptions, and
limitations will also be described.
Definition and Scope of the Problem
Hypertension is defined as systolic BP (SBP) of 140 mmHg or greater, diastolic
BP (DBP) of 90 mmHg or greater, or taking antihypertensive medication. In the United
States, people with hypertension comprise a rapidly growing subset of the population.
Approximately 50 million Americans have high BP. High BP was the primary cause of
death for 44,435 Americans in 1998 and contributed to about 210,000 deaths (American
Heart Association [AHA], 2003b). Approximately 95% of people with hypertension
have essential (or primary) hypertension, for which no clear cause can be identified.
From 1987 to 1997, the death rate from high BP increased by 13.1% (AHA, 2000).
Treatment of hypertension continues to be plagued by dismal statistics in that only 27.4%
of Americans with high BP are adequately controlled on medication (AHA, 2003a).
Elevated systolic BP (SBP) specifically has been associated with increased
morbidity and mortality, especially in the older population. Prospective studies have
shown that there is a strong, continuous, graded, independent association between SBP
and the risk of coronary heart disease, stroke, and end-stage renal disease (He &
Whelton, 1999). Additionally, data from the National Health and Nutrition Examination
Survey (NHANES) III found that isolated systolic hypertension was the most frequent
subtype of uncontrolled hypertension, especially in subjects over 50 years of age
(Franklin, Jacobs, Wong, L'Italien, & LaPuerta, 2001). The incidence and severity of
complications increase with the duration and severity of hypertension (Kaplan, 1998;
Lackland, 2000). Because of this, it is crucial to identify and treat high BP, and
specifically high SBP, in order to reduce the risk of advanced cardiovascular disease and
its associated morbidity and mortality.
Inadequate adherence to antihypertensive therapy is a major challenge and
contributes to elevated BP levels in two-thirds of all patients with hypertension (JNC VI,
1997). One of the major obstacles in the diagnosis and treatment of hypertension is that
it has a very insidious course, which the patient often fails or refuses to recognize
because he or she may continue to "feel good." Noncompliance with antihypertensive
therapy has been cited as the major cause of treatment failure (AHA, 2003c).
Noncompliance is a multi-faceted issue that results from varying behavioral,
social, logistical, economic, and practical factors (Miller, Hill, Kottke, & Ockene, 1997).
Failure to comply with prescribed medication regimens or other therapies can affect
patients' health adversely as patients may fail to improve, worsen, or relapse.
Compliance not only affects the immediate patient but the entire United States health
care system and economy. Noncompliance accounts for 100 billion dollars in health care
and productivity costs in the United States. The costs of hospitalizations and practitioner
visits caused by noncompliance account for 8.5 billion dollars annually (Task Force for
Several factors have been associated with antihypertensive adherence patterns
including whether or not symptoms affect daily life or work, family history of
hypertension, household composition, perceived threat of complications, and perceived
need and perceived effectiveness of medications (McLane, Zyzanski, & Flocke, 1995;
Meyer, Leventhal, & Gutmann, 1985). Because hypertension is generally thought of as
an asymptomatic disease and due to the lack of definitive symptoms associated with high
BP, it can be difficult for patients to adequately prescribe meaning and importance to
their disease process and treatment options (McLane et al., 1995). If high BP were
associated with observable symptoms, it may be possible to improve early recognition of
the disease, improve its treatment compliance and improve outcomes.
Over the past several years, more attention has been paid to preventive health
care and patients have been viewed more in terms of being healthcare consumers and less
as being passive participants of the healthcare process. Noncompliance in the patient
with hypertension comes in the face of growing consumer empowerment among patients
(Skelton, 1997). More than ever, people are trying to improve their health by
participating in their care (Roter, Stashefsky-Margelit, & Rudd, 2001). In addition to
pharmacologic therapy, biofeedback therapy has been used successfully to assist people
in treating and preventing major health problems, such as hypertension, chronic pain, and
anxiety (Fernandez & Beck, 2001; Knost, Flor, Birbaumer, & Schugens, 1999; Lal et al.,
1998). Biofeedback therapy has been used successfully in both research and clinical
settings to lower BP in hypertensive patients (Lal et al., 1998; Yucha et al., 2001). These
therapies would be strengthened if patients were more aware of their high BP or if they
had symptoms associated with high BP that could be coupled with therapy. Healthy
People 2010 identified goals to advance the prevention, detection, and treatment of
hypertension, stroke, and heart disease. To increase public attention, awareness, and
treatment, goal number 12-12 states that there "should be an increase in the proportion of
adults who have had their BP measured within the preceding 2 years and can state
whether their BP was normal or high" (Healthy People 2010, 2003).
As patients with hypertension strive to become more involved in their healthcare
decisions, treatments need to be found that focus on the patient as the manager of his/her
own health. High BP is a phenomenon that generally is not associated with specific
symptoms or signs (AHA, 2003c). Because of this, patients with hypertension often have
difficulty understanding the threat of the disease or the treatments required to manage the
disease. In disorders with observable symptoms, such as diabetes mellitus, congestive
heart failure or seizures, patients may be more motivated to seek and continue treatment.
Little is known about the extent to which hypertensive patients are aware of their
high BP; however, several research studies and clinical experiences have shown that
people can be more aware of their BP levels after different types of feedback training. If
patients were aware of their high BP episodes, better-tailored treatment modalities may
be developed and adherence to therapeutic treatment may be improved resulting in better
patient outcomes. For example, biofeedback or relaxation therapies could be used to
assist patients in lowering their BP during episodes of high BP.
While there is continued controversy over whether there are definitive symptoms
associated with BP, it is generally believed that most patients with hypertension cannot
accurately tell if their BP is elevated (Fahrenberg, Franck, Baas, & Jost, 1995).
However, some clinicians and researchers report that certain patients are able to detect
when their BP is elevated (Barr, Pennebaker, Watson, 1988). These patients often report
vague symptoms that are associated with their high BP. Symptoms such as headache,
racing heart, sweaty hands, cold/warm hands, tight stomach, muscular tension, dizziness,
blurred vision, lightheadedness, tension, palpitations, flushed face, and warm/cold
extremities have been correlated with variations in BP (Bulpitt, Dollerly, & Came, 1976;
Pennebaker, Gonder-Frederick, Stewart, Elfman, & Skelton, 1982).
There are many hypotheses behind the development and maintenance of
hypertension. These theories provide a framework for understanding how patients with
high BP can be helped to recognize the subtle signs and symptoms. One hypothesis of
hypertension development is the sympathetic nervous system theory of hypertension
development. This hypothesis describes hypertension as a result of over-stimulation of
the SNS. To substantiate SNS overactivation, several studies of patients with essential
hypertension demonstrate increased levels of plasma norepinephrine and elevated
norepinephrine spillover. Patients with borderline and essential hypertension have an
increased sympathetic and a decreased parasympathetic drive (Rahn, Barenbrock, &
Hausberg, 1999). It is hypothesized, and highly debated, whether sympathetic nervous
system (SNS) activation is a trigger for high BP (defense reaction) or if SNS activation is
due to a secondary phenomenon (e.g., endothelial or baroreceptor dysfunction).
Alterations and/or uncompensated increases in SNS activity in hypertensives may cause
subtle physical signs and symptoms. Increased SNS activity and early hypertension are
often characterized by an increased heart rate, cardiac output, and renal vascular
resistance. The sympathetic nervous system elicits a "fight or flight" response when
confronted with a stimulus, such as when the person is in an emergency or stressful
situation. Additionally, symptoms that are related to increased SNS activity have been
reported in hypertensives and have been correlated with high BP episodes (Carels,
Sherwood, & Blumenthal, 1998).
Potential manifestations of increased SNS activity include increased heart rate
and stroke volume (cardiac output), increased cardiac contractility and venous return,
renal retention of sodium and water, increased thirst, increased venous tone, increased
angiotensin II, increased peripheral resistance, increased local vasoconstrictors/regulators
(e.g., endothelin), increased blood viscosity, and decreased local vasodilators/regulators
(e.g., nitric oxide). Symptoms associated with high BP may be related to overstimulation
or oversensitivity of the SNS in hypertensive individuals (Esler, 2000; Kaplan, 1998;
Rahn, Barenbrock, & Hausberg, 1999).
It has been reported that individuals, both normotensive and hypertensive,
estimate their BP levels by using both internal sensory and external situational
information (Barr et al., 1988). Estimations and beliefs about BP levels may or may not
be accurate, but they are important because people act upon them. In fact, Pennebaker et
al. (1982) suggest that variations in BP are correlated to different symptoms and that a
person can monitor his or her BP by monitoring symptoms. Interestingly, in studies
where both normotensive and hypertensive people were asked to estimate their BP levels,
estimated BP was strongly associated with symptoms and moods (Baumann & Leventhal,
1985) and with feelings of physical tenseness and physical activity (Fahrenberg et al.,
Several studies on whether or not people can accurately estimate their BP have
been performed. The findings have been fraught with much speculation and conflicting
results (Barr et al., 1988; Baumann & Leventhal, 1985; Brondolo, Rosen, Kostis, &
Schwartz, 1999; Cinciripini, Epstein, & Martin, 1979; Fahrenberg et al., 1995;
Greenstadt, Shapiro, & Whitehead, 1986; Luborsky et al., 1976; Shapiro, Tursky, &
Schwartz, 1970). An important variable among these studies was the addition of a
feedback intervention. Among the feedback intervention-type studies, all showed an
improvement in BP discrimination after feedback (Barr et al., 1988; Brondolo et al.,
1999; Cinciripini et al., 1979; Greenstadt et al., 1986; Luborsky et al., 1976; Shapiro et
Different types of feedback have been used to assist subjects in learning to
recognize symptoms, situations, and factors that are associated with their BP levels.
Barr, Pennebaker, and Watson (1988) provided normotensive subjects actual
biosituational factors (e.g., symptoms, moods, situations) that were related to their SBP
levels. They found that 71.4% of the subjects in the biosituational feedback group had
significant accuracy correlations compared with 31.3% of the subjects in the control (no
feedback) group. Additionally, providing normotensive (Barr et al., 1988; Cinciripini et
al., 1979; Greenstadt et al., 1986) and hypertensive subjects' (Brondolo et al., 1999
Luborsky et al., 1976; ) knowledge of their actual BP levels has also been used to
improve accuracy in estimating BP levels.
Because of the continued prevalence and incidence of hypertension and its
complications, there must be more research focused on testing detection and intervention
strategies, as well as improving patient compliance (AHA, 2003c; Miller, Hill, Kottke, &
Ockene, 1997). The American Heart Association Expert Panel on Compliance (Miller et
al., 1997) reported that a multilevel approach featuring both behavioral and educational
strategies was needed to assist patients and providers in improving compliance (Miller,
Hill, Kottke, & Ockene, 1997).
Because the majority of BP feedback intervention-type studies have been
performed on normotensive, healthy volunteers, it is unknown whether adults with
hypertension can accurately estimate their BP or if this awareness can be improved
through BP or biosituational feedback. Specifically, it is unknown if hypertensive adults
can estimate their SBP more accurately after participating in ambulatory BP feedback
and biosituational self awareness training.
Purposes of the Study
The purposes of the study are as follows:
1. To determine if there are differences in the mean absolute difference (AD)
among adult hypertensives after training compared to before training.
2. To determine if there are differences in the mean improvement of
estimating SBP among college-educated hypertensives versus noncollege-
3. To determine if college-educated hypertensives decrease their mean AD
posttraining compared to pretraining.
4. To determine if there are differences in the mean improvement of
estimating SBP between hypertensives whose body mass index (BMI) is >
30 and hypertensives whose BMI is < 30.
5. To determine if there are differences in the mean improvement of
estimating SBP between male hypertensives and female hypertensives.
6. To determine if there are differences in the mean improvement of
estimating SBP between hypertensives who are < 48 years of age
compared with those who are > 48 years of age.
7. To determine if there are differences in the mean improvement of
estimating SBP between hypertensives who use antihypertensive
medications and those who do not use antihypertensive medications.
The hypotheses investigated are listed below:
1. Adult hypertensives differ significantly in their mean improvement of
estimating SBP after the ambulatory BP awareness training intervention,
compared with before the training intervention.
2. College-educated hypertensives differ significantly from noncollege-
educated hypertensives in their mean improvement of estimating SBP.
3. College-educated hypertensives decrease their mean AD posttraining
compared to pretraining.
4. Hypertensives with a BMI < 30 differ significantly from hypertensives
with a BMI > 30 in their mean improvement of estimating SBP.
5. Male hypertensives differ significantly in their mean improvement of
estimating their SBP compared to female hypertensives.
6. Hypertensives < 48 years of age differ significantly in their improvement
of estimating SBP compared to hypertensives > 48 years and older.
7. Hypertensives using antihypertension medication differ significantly in
their mean improvement of estimating SBP compared with hypertensives
not taking medications.
Definitions of Terms
The absolute difference (AD) is defined as the absolute value of the mean
difference between actual and estimated SBP. The absolute difference was calculated for
mean actual SBP days 1, 2 and 3, and 4 and mean estimated SBP days 1, 2 and 3, and 4.
Actual SBP is defined as that which is measured using the ambulatory BP
monitor; it is viewed as a continuous variable with parameters defined as mean, standard
deviation, and variance.
Ambulatory BP feedback is defined as those BP readings from the ambulatory BP
monitor that can be viewed by the patient on the unblinded LCD screen.
Ambulatory BP monitoring is defined as an automatic, noninvasive cuff-
oscillimetric recorder (Model 90207, SpaceLabs, Inc., Redmond, WA) which measures
ambulatory BP. Subjects wear the ambulatory BP monitor cuff in a similar fashion as a
standard manual sphygmomanometer. However, the ABP monitor is preprogrammed via
specialized software to automatically measure BP at preset intervals throughout the day
and night. The subject wears the cuff around his/her upper forearm and the main unit is
strapped around the waist via a strap or belt. ABP monitoring is a reliable and
naturalistic method for obtaining BP readings while subjects are in their normal
Biosituational feedback is defined as feedback related to biological, situational,
psychological factors that the subject has experienced. Biosituational feedback in this
study is provided to the subject by providing the subject with information on their actual
SBP, self-reports of their estimated SBP, and self-reports of their moods, symptoms, and
activities during BP measurement.
A blinded-LCD screen is the panel on the ABP monitor that displays the time of
day, but does not display the physiologic data (i.e., the patient cannot view the BP
Estimated SBP is defined as that which is estimated by each subject; it is viewed
as a continuous variable.
Hypertension is defined as SBP of 140 mmHg or greater, diastolic BP of 90
mmHg or greater, and/or taking antihypertensive medication.
Hypertensive subjects are identified as hypertensive if they have BP readings
greater than 140/90 on both of the two screening BP measurements or they are taking
The mean improvement is defined as the absolute value of the mean difference of
day 1 (mean actual SBP minus mean estimated SBP) minus the absolute value of the
mean difference of day 4 (mean difference of actual SBP minus estimated SBP).
An unblinded-LCD screen is the panel on the ABP monitor that displays the time
of day and allows the subject to view the SBP, DBP, and heart rate.
The following assumptions were made in this study:
1. Participants have some knowledge of their health status, including BP and ways
to treat high BP.
2. Participants have some opinions about their BP patterns and factors relating to
their high BP.
3. Participants have access to various sources of information about high BP.
4. Participants may have symptoms and patterns that are associated with their high
5. People with high BP may have alterations in autonomic nervous system
functioning that may predispose them to have symptoms during high BP episodes.
6. Symptoms, patterns, and causes of high BP vary from person to person.
7. Patients with hypertension have variability in their SBP of at least 30-50 mmHg
in a 24-hour period.
The generalizability of the results of this study is limited to adult hypertensive
persons who live in the North Central Florida area. Despite this limited geographic
range, the population is believed to be similar to the population of hypertensive persons
in other parts of the United States.
Significance of the Study
Hypertension is a major cause of death in the U.S. and worldwide. Only about
one quarter of adults with hypertension are being adequately controlled on medications
(AHA, 2003c). Because of this, there will be increased economic burden and increased
morbidity and mortality associated with high BP. Hypertension is difficult to treat for a
variety of reasons. One issue is that hypertension is a relatively asymptomatic disorder
and patients may not even realize that their BP is elevated. Because there has been
limited research inquiry into hypertensives' awareness of their BP levels, it is generally
unknown whether hypertensives can improve their ability to estimate their BP. Research
has indicated that SBP is an important determinant to the risk of coronary heart disease,
stroke, and end-stage renal disease (He & Whelton, 1999). Because of the importance of
SBP prediction and modification, this study examined the ability of adult hypertensive
persons to estimate their SBP before and after a biosituational feedback training
intervention. A better understanding of estimation of SBP among hypertensives will
encourage researchers to study and develop new and better-tailored treatment modalities.
This study also utilized ABP monitoring and a self-report diary to assist adults with
hypertension to learn more about their BP patterns and associated factors. Finally, this
study examined differences between different groups of hypertensives. This information
will shed light on potential sub-groups that may be better or worse at estimating their
SBP and may encourage a more focused inquiry into SBP estimation and biosituational
feedback training. Additionally, if hypertensives can improve their ability to estimate
their SBP levels, there may be improved adherence to medications, improved
hypertension therapies, and improved outcomes.
REVIEW OF LITERATURE
This chapter will present a literature review of the following areas of research:
theories of hypertension development, systolic hypertension, role of sympathetic nervous
system in hypertension, issues surrounding the treatment of hypertension, biosituational
factors associated with high BP, BP estimation, and ambulatory BP monitoring. A
summary linking these areas together to provide a research rationale for this study will
conclude this chapter.
Theories of Hypertension Development
There have been several mechanisms that have been implicated in hypertension
development. These mechanisms include impaired baroreceptor function, increased
sympathetic nervous system activity, impaired endothelial function, and/or structural-
adaptive changes in the vascular walls.
Impaired Baroreceptor Function and Baroreceptor Resetting
The baroreceptor mechanism in the central nervous system assists with the
regulation and control of arterial pressure. Baroreceptors are nerve endings that lie in the
walls of large arteries and are stimulated when stretched. This reflex is initiated by
pressure-sensitive receptors, located in the walls of the large arteries of the neck and
thoracic regions, carotid artery, and the aortic arch. The baroreceptors respond rapidly to
acute drops or elevations in BP. The baroreceptor signal is transmitted, enters the
medulla, and stimulates either the sympathetic nervous system (SNS) (if BP is too low)
or the parasympathetic nervous system (PNS) (ifBP is too high). Stimulation of the SNS
promotes the secretion of both norepinephrine (NE) and epinephrine and causes
vasoconstriction in vascular smooth muscles and blood vessels and increased strength of
heart contraction. Stimulation of the PNS would promote the secretion of acetylcholine
and cause vasodilation of the veins and arterioles and decreased heart rate and strength of
contraction. The baroreceptor mechanism is an extremely powerful and effective entity
within the nervous and cardiovascular systems for short-term regulation of BP
(Chapleau, Cunningham, Sullivan, Watchel, & Abboud, 1995; Harrington, Murray, &
Ford, 2000; Seeley, Stephens, & Tate, 1998).
One of the problems with the baroreceptor system in the long-term regulation of
arterial pressure is that the baroreceptors are continually "reset" after 1 to 2 days of
prolonged pressure exposure. Consequently, they are only effective if the change in BP
is acute or not prolonged. For example, if the pressure rises from the normal 100 mmHg
to 170 mmHg, there would be an acute and immediate response from the baroreceptor
reflex (vasodilation). The rate of impulse firing is rapid and extremely acute, and then
diminishes over the course of a few seconds. The rate of impulse firing continues to
decline over a period of 1 to 2 days until ultimately the rate of firing ceases, despite the
fact that the arterial pressure remains at 170 mmHg. Thus, the baroreceptor has been
"reset" to be accustomed to a consistently high BP level (Chapleau et al., 1995; Guyton
& Hall, 1996).
It is interesting to note that studies have shown that young, mild or borderline
hypertensive patients have an increase in BP variability and skeletal muscle sympathetic
nerve activity, and display increased baroreceptor activity. This may be a compensatory
finding that is associated with increased sympathetic nerve activity, whereby the
baroreceptors are attempting to adjust the BP toward more normal levels. In established
hypertension associated with myocardial hypertrophy and decreased myocardial stretch-
ability, baroreceptor function has been shown to decline (Chapleau et al., 1995).
The baroreceptor reflex may also not be effective in long-term regulation of BP
because of the structural and functional changes that are seen in the blood vessels of
patients with hypertension. Because of the anatomical location of the baroreceptor nerve
endings, dysfunction of the vessel lumen/endothelium may decrease the baroreceptor
pressure-sensor effectiveness (Chapleau et al., 1995; Seeley et al., 1998).
Another problem of short- and long-term baroreceptor regulation of arterial BP is
that even under conditions of "normal" aging, baroreceptor function and other
cardiopulmonary neural regulatory functions have been shown to be less effective with
age. In animal studies, the effects of administration of acetylcholine on heart rate
(i.e., bradycardia) are more pronounced in elderly normotensive subjects than in younger
controls. The baroreceptor control of BP in normal subjects is reported to be comparable
to that of the younger controls; however, the response to the stimulus (either high or low
BP) is sluggish and slower. Thus, baroreceptor control of BP becomes impaired with the
aging process, however to a lesser degree than heart rate regulation. Studies have also
shown that there is impairment in the cardiogenic stretch receptors located in the
cardiopulmonary region that are associated with aging (Chapleau et al., 1995; Fauvel et
al., 2000; Giannattasio et al., 1994). Impaired baroreceptor function and baroreceptor re-
setting may lead to uncompensated increases or decreases in BP. It remains unclear
whether baroreceptor dysfunction is the cause or effect of hypertension.
Sympathetic Hyperactivity Theory
In the sympathetic hyperactivity theory of hypertension, hypertension is caused
by an abnormally increased stimulation of the sympathetic nervous system. Increases in
catecholamine stimulation effect BP by increasing heart rate, stroke volume, and
peripheral resistance. Factors that may be associated with increased sympathetic outflow
and increased total peripheral vascular resistance in essential hypertension include
baroreflex re-setting; genetic composition; stress; altered renin-angiotensin-aldosterone
mechanisms; alterations in circulating hormones/substances; structural-adaptive changes
in vascular walls; endothelial dysfunction; endothelial derived relaxing and contracting
factors; and membrane and intracellular mechanisms, including impaired adrenergic
receptor numbers and types. The increase in SNS activity stimulates the release of
catecholamines to effect specific target organs including the vascular smooth muscle,
blood vessels, kidneys, and heart. Effects of increased SNS activity include increased
heart rate and stroke volume (cardiac output), increased cardiac contractility and venous
return, renal retention of sodium and water, increased thirst, increased venous tone,
increased angiotensin II, increased peripheral resistance, increased local
vasoconstrictors/regulators (i.e., endothelin), increased blood viscosity, and decreased
local vasodilators/regulators (i.e., nitric oxide) (Lilly, 1998).
Folkow (1982) proposed a "defense-reaction" theory of increased sympathetic
activity in hypertension. Folkow hypothesized that certain individuals may undergo
defense reactions to conditioned stimuli on a daily basis; without the actual fight-or-flight
reaction, and this would in-turn cause marked increases in sympathetic activity. If the
conditioned stimuli were continually repeated, adverse structural adaptive changes of the
arterioles would occur, thus leading to the further development of sustained hypertension
(Brondolo, Karlin, Alexander, Borrow, & Schwartz, 1999; Carels et al., 1998; Folkow,
2000; Wright & Angus, 1999).
In numerous studies of young patients with essential hypertension, it has been
shown that there are increased levels of plasma norepinephrine and elevated
norepinephrine spillover (Esler, 2000; Grassi et al., 2000; Rahn et al., 1999). In a study
by Egan, Panis, Hinderliter, Schork, & Julius (1987), mildly hypertensive young humans
had elevated plasma norepinephrine levels and enhanced skeletal muscle vasoconstrictor
tone. These findings provide understanding of the hemodynamic profile of early human
hypertension, which is characterized by increased heart rate, cardiac output, and renal
vascular resistance. Increased sympathetic activity has also been shown to be a factor in
elderly hypertension. In a study by Grassi et al., (2000), muscle sympathetic nerve
activity was increased in 20 untreated elderly essential hypertension patients compared
with age-matched controls. In addition to subjects with existing hypertension,
normotensives with a family history of hypertension have higher rates of norepinephrine
spillover into arterial plasma than do normotensives without a family history of
hypertension. This finding may be a contributing factor and provide a link for the later
development of hypertension. It was also reported that patients with accelerated essential
hypertension have significantly higher levels of muscle sympathetic nerve activity than
do patients with milder hypertension. There have been several proposed mechanisms for
increases in muscle sympathetic nerve activity in essential hypertension. One such
proposal is that increases in muscle sympathetic nerve activity may be related to
increased central nervous system sympathetic outflow. Another such hypothesis is that
patients with essential hypertension have impaired baroreflex sensitivity (Mark, 1996).
Increased sympathetic activity and enhanced reactivity to stress have been
reported in patients with both borderline and established hypertension, and it has been
suggested that they play a role in the pathogenesis of hypertension. The mechanism for
these enhanced responses is unknown; however, it has been suggested that epinephrine,
released from the adrenal medulla during physiological stress, is taken up into the
sympathetic nerve terminal and later released as a co-transmitter with norepinephrine.
The norepinephrine that has been released further stimulates norepinephrine release
through its action on the presynaptic B-adrenergic receptors. In a recent study,
hypertensive subjects had a 25% higher rate of whole body spillover of norepinephrine to
plasma, compared to normotensive controls. Additionally, the epinephrine secretion rate
was increased in hypertensives (215 +/- 209ng/min) versus normotensives (173 +/- 115
ng/min). These findings provide evidence the epinephrine may prolong and amplify the
sympathetic responses at a time when circulating ephinephrine concentrations are no
longer elevated (Rumantir et al., 2000; Stein, Nelson, He, Wood, & Wood, 1997).
There have also been studies that demonstrate differences in SNS activity among
subsets of the population. Stein, Lang, Singh, He, and Wood (2000) reported that
healthy, normotensive black males (compared to age-matched white males) had
markedly increased levels of vascular sensitivity to an infusion of the alpha-adrenergic
vasoconstrictor substance, phenylephrine (Stein et al., 2000). This study concluded that
increased sympathethetically-mediated vascular tone caused by enhanced
vasoconstriction and attenuated vasodilation may play a role in the pathogenesis of
hypertension in blacks. It has also been reported that obese-normotensive and obese-
hypertensive subjects have impaired adrenergic and baroreflex function. In a recent
study, Grassi et al. (2000) reported that muscle sympathetic nerve activity is significantly
increased in lean hypertensive and overweight normotensive subjects (p = 0.01),
compared to lean normotensive control subjects. Additionally, obese-normotensive and
obese-hypertensive subjects had impaired baroreflex cardiovascular control, as measured
by the infusion ofvasoactive drugs (nitroprusside and phenylephrine) and the response of
each substance. This study concluded that the association between obesity and
hypertension triggers a sympathetic activation and an impairment in baroreflex control
mechanisms (Grassi et al., 2000; Julius, Valentini, & Palatini, 2000).
The endothelium is closest to the arterial lumen, in the intimal layer, and intimate
with blood flow. In the normal artery, the endothelium functions to maintain the
integrity of the vessel wall by performing various metabolic and signaling functions. The
endothelium functions to (a) act as a barrier and protect subendothelial space, (b) express
antithrombogenic substances (heparin, thrombomodulin, plasminogen activitators), (c)
secrete vasoactive substances that promote vasodilation (endothelium-derived relaxing-
factor and prostacyclin), and (d) inhibit smooth muscle cell migration and proliferation
by secretion of heparin and endothelium-derived relaxing factor. Atherosclerotic lesions
develop within the intimal layer (Lilly, 1998; Luscher, 1994).
Over the last several years, increasing attention has been paid to a substance
secreted by the endothelium known as Endothelium-derived-relaxing-factor (EDRF), also
known as Nitric Oxide (NO). In addition to its vasodilatory properties, NO is known to
inhibit platelet aggregation and adhesion, monocyte adherence and chemotaxis, and
proliferation of vascular smooth muscle cells. Endothelium-derived nitric oxide, a potent
vasodilator, may be an endogenous antiatherogenic factor. In animal and human models,
vasodilation caused by the release of endothelium-derived NO is diminished in
atherosclerotic vessels. In addition, hypercholesterolemia independent of observable
atherosclerosis inhibits endothelium-dependent vasodilation. In addition to NO, the
endothelium also produces potent vasoconstrictor substances including endothelin-1.
The expression of endothelin-1 is stimulated by factors including thrombin, angiotensin-
II, epinephrine, and the shear stress of blood flow (Chowdhary et al., 2000; Lilly, 1998;
Because of the protective nature of the endothelium, it is important that the
integrity of the endothelium be intact. In response to some type of "injury" to the
endothelial layer, the endothelium undergoes a continuum of changes that adversely
affect the structural and functional physiology of the endothelial surface. Injured
endothelium demonstrates increased permeability to large molecules and substances
under the subendothelial space, reduced antithrombotic properties and increased
vasoconstriction due to decreased secretion of prostacyclin and EDRF-NO, and increased
smooth muscle cell migration and proliferation due to decreased secretion of EDRF-NO
and platelet-derived growth factor (PDGF). Atherosclerosis is a disease of the muscular
arteries (e.g., aorta, coronary and cerebral vessels) in which the intimal layer becomes
"injured" and thickened by fatty deposits and fibrous tissue. Elevated levels of serum
cholesterol aggravate the vessel endothelium integrity and cause changes within the
vessel lumen. The earliest visible lesion of atherosclerosis is a fatty streak characterized
microscopically by the subendothelial accumulation of large, lipid-laden "foam cells."
Foam cells are derived from macrophages and smooth muscle cells (SMC's). Factors
involved in monocyte migration and accumulation in the subendothelial space include
increased levels of serum cholesterol, especially low-density lipoproteins (LDLs) and
oxidized LDLs which encourage the presence of adhesion molecules and chemotactic
proteins. Once in the subendothelial space, the monocytes become activated
macrophages and release mitogens and chemoattractants (including tumor necrosis
factor, interleukins, complement fragments, PDGF, immune complexes, smooth muscle
cell growth factors, and monocyte chemo-attractant proteins) that recruit additional
monocytes and promote SMC growth and clot promotion. In advanced disease, a fibrous
plaque of SMC origin develops in the intimal layer when there is continual accumulation
of monocytes, lymphocytes, foam cells, and connective tissue. Complications occur due
to weakening of the vessel wall, ulceration of the vessel wall, occlusion of vessel lumen,
thrombosis and distal embolization (Chalmers, 2000; Lilly, 1998; Luscher, 1994;
Schwartz, Reidy, & De Blois, 1996).
Hypertension probably is a risk factor of endothelial dysfunction, as increases in
sympathetic nervous system activity have been shown to injure vascular endothelium and
may increase the permeability of the vessel wall to lipoproteins and other atherogenic
factors (Lilly, 1998; Toikka et al., 2000). Because endothelin-1 is stimulated by
mechanisms that are affected by increased SNS activity and a majority of patients with
hypertension have clinically increased SNS activity, it could be possible that these
factors may influence peripheral resistance, and therefore BP. In addition, decreases in
endothelium-derived vasodilating and increases in endothelium-derived constricting
factors cause an increase in BP and vascular resistance and this may be a risk factor for
hypertension development. In a recent study by Park, Charbonneau, and Schiffrin
(2001), endothelial dilatory responses to acetylcholine infusion in the brachial artery
correlates with the presence of endothelial dysfunction in human resistance arteries. In
this study, endothelial-dependent dilatory responses were found to be similar in large and
small arteries in hypertensive patients. This conclusion suggests that endothelial
dysfunction may have a systemic rather than a local nature in atherosclerosis and
hypertension (John & Schmieder, 2000; Park et al., 2001).
Endothelial dysfunction, atherosclerosis, and/or hyperlipidemia may also
precipitate alterations in the integrity of the protective endothelium and thereby increase
vasoconstrictor substances, leading to hypertension. Hypothetically, if a person had early
atherogenesis and/or hypercholesterolemia but no hypertension, he/she may have
impaired EDRF-NO function and increased endothelin-1 stimulation and therefore may
have increases in systemic BP (Lilly, 1998; Park et al., 2001).
Baroreceptor function may be modulated by factors such as prostacyclin, oxygen-
free radicals, and factors released from aggregating platelets (Chapleau et al., 1995).
Endothelial dysfunction and subsequent altered release of these factors contribute
significantly to the decreased baroreceptor sensitivity in hypertension and
atherosclerosis. Dysfunctional changes in the endothelium may impair baroreceptor
function by reducing the stretch mechanisms that provide signals to the autonomic
nervous system. Chapleau et al. (1995) reported that the inhibition of endogenous
formation of prostacyclin and increased platelet aggregation reduced baroreceptor
activity in healthy rabbits. Additionally, oxygen free-radical generation (as seen in
atherosclerotic lesions and oxidized-LDL) suppressed baroreceptor activity in the normal
carotid sinus (Chapleau et al., 1995).
As mentioned previously, various structural and functional changes occur within
the vessel wall that may encourage the development and maintenance of hypertension.
Structural and adaptive changes that occur in the vessel wall and cardiovascular system
include vascular and left ventricular hypertrophy, arterial stiffness, decreased vessel
compliance, and atherosclerosis of the coronary and carotid arteries. In a study
comparing age-matched borderline versus normotensive subjects, increased carotid and
brachial intima-media thickness was seen in the borderline hypertensive group. In
addition, oxidized-LDL was increased in the borderline hypertension group compared
with the control group (Toikka et al., 2000). Interestingly, a study of moderately
hypercholesterolemic and hypertensive subjects reported that systolic BP and pulse
pressures are associated with alterations in increased carotid-intimal thickening
(Zanchetti et al., 2001).
Structural and functional changes that occur in the pathophysiological processes
of atherosclerosis, SNS overactivation, and endothelial dysfunction can impair baroreflex
function (Chapleau et al., 1995), impede blood flow, increase resistance of flow, increase
BP, and can encourage a number of advanced adverse complications of hypertension
including thrombosis formation, stroke, myocardial infarction, renal failure, retinopathy,
and death. It is interesting to note, however, that human vessels can undergo massive
accumulations of atherosclerotic plaque without narrowing of the lumen. This may be
due to compensatory remodeling of the vessel wall and dilating to permit a normal level
of blood flow. In studies of balloon-injured rabbit carotid arteries, researchers found no
narrowing of the vessel lumen despite an increase in wall thickness (Schwartz et al.,
1996). Increased sympathetic adrenergic activity can also increase arterial stiffness and
decrease vessel compliance. Increased workload on the heart induced by hypertension
and/or SNS activity causes hypertrophy of the left ventricle and decreased compliance of
the ventricle to properly fill and contract blood. The level of arterial pressure exerts an
important influence on the level of left ventricular muscle mass. Approximately 20% to
35% of variability in LV mass can be predicted from the level of 24-hour ambulatory
BPs (Devereux, de Simone, Ganau, & Roman, 1994).
In summary, it is clear that there are many factors that are related to hypertension
development and maintenance. Hypertension development and maintenance is most
likely extremely individual and probably a function of a combination of the discussed
mechanisms and alterations. Because of the complex nature of the vasculature,
circulatory, and neurological systems, each of these theories impacts SNS activity and
thereby could promote hypertension development and maintenance.
For the purposes of this study, the SNS hyperactivity theory of hypertension
development will be explored as a possible link between high BP and high BP
recognition. In the SNS hyperactivity theory of hypertension, high BP is caused by an
abnormally increased stimulation of the SNS. The exact mechanism for increased SNS
activity in hypertension is largely unknown, but has been speculated by researchers
(Folkow, 1982). As mentioned previously, the increase in SNS activity stimulates the
release of catecholamines to affect specific target organs including the vascular smooth
muscle, blood vessels, kidneys, and heart. Stimulation of the SNS causes physiological
manifestations, such as racing heart, pounding chest, increased BP, and dilated pupils.
Studies show that there are increased levels of plasma norepinephrine and
elevated norepinephrine spillover in essential and borderline hypertension, seen in both
younger and older hypertensives (Egan et al., 1987; Esler, 2000; Grassi et al., 2000; Rahn
et al., 1999;). Because age has been shown to be a factor in increased SNS activity, it
would seem plausible that adults of increased age or younger borderline hypetensives
would have increased SNS output and therefore potentially more manifestations of SNS
activity. Similarly, adults who are obese have been shown to have impaired adrenergic
and baroreflex function (Grassi et al., 2000). Therefore, obese adults may have physical
signs or symptoms associated with BP elevation. Whether or not this activity occurs
only during a high BP episode or if it occurs more consistently is unknown. It is also
unknown whether obese or elderly hypertensives have an increased recognition or
awareness of high BP or high levels of sympathetic activity.
The majority of persons with systolic hypertension are not adequately controlling
their BP levels despite persuasive data from clinical trials documenting the benefit of
treatment (JNC VI, 1997, p. 6). Systolic BP has been identified as a major measure in
the assessment of risk in hypertensive subjects (Lackland, 1999). Observational
epidemiologic studies and randomized controlled trials have demonstrated that SBP is an
independent and strong predictor of risk of cardiovascular and renal disease (Franklin et
al., 2001; He & Whelton, 1999). Recent data from the Systolic Hypertension in the
Elderly Program (SHEP) have indicated a clear benefit of treatment with a reduction in
total stroke of 36%, and a reduction of 25% and 32% in the combined end points of
coronary heart disease and cardiovascular disease, respectively (Silagy & McNeil, 1992).
SBP levels have been shown to covary more with physical symptoms than either
DBP or heart rate (Pennebaker et al., 1982). From a perspective of training patients to
recognize high BP episodes, it has been shown that discrimination of systolic pressures
occurs at a slightly faster pace than diastolic pressures (Cinciripini et al., 1979). It also
may be easier for subjects to understand the estimation task as well as minimize
confusion between SBP and DBP levels, thereby increasing the reliability of the SBP
estimate. Because of the importance of SBP as a predictor in long-term outcomes and
the ease of conceptualization, it is valuable to solely examine the ability of hypertensive
persons to estimate their SBP levels.
Issues Surrounding the Treatment of Hypertension
Overview of Treatment Statistics in High BP
A goal of therapy for patients with hypertension as defined by the JNC VI report
(1997) is to reduce BP to nonhypertensive levels with minimal to no side effects.
According to recent estimates from the American Heart Association (AHA), one in four
U.S. adults has high BP, but because there are no symptoms, nearly one-third of these
people don't even know they have it. The current goal for BP is to have BP controlled to
less than 140/90 mm Hg. However, it is estimated that only 26.2% of people with high
BP are on antihypertensive medications but do not have it under control. For a historical
perspective, in 1972, 16% of high BP patients were controlled to less than 160/95 mm
Hg, the goal at the time. A recent AHA survey indicated that the control rate for today's
goal of less than 140/90 mm Hg is 29% (AHA, 2003a). Thus, it would seem that we are
making progress, but we have a long way to go. The economic burden of uncontrolled
hypertension is immense. For example, researchers estimated the number of cases and
costs of myocardial infarction, stroke, and congestive heart failure for patients achieving
BP control versus those not achieving control. For the U.S. population with hypertension,
inadequate BP control was estimated to result in 39,702 cardiovascular events, 8,374
cardiovascular disease deaths, and $964 million in direct medical expenditures. Within
the medicated population with cardiovascular disease, the incremental costs of failure to
attain BP goals reached approximately $467 million. These results reflect the importance
of adequate BP control, in particular, systolic BP control, in reducing cardiovascular
morbidity, mortality, and overall health care expenditures among patients with
hypertension (Flack et al., 2002).
Poor adherence to antihypertensive therapy is a major therapeutic challenge
contributing to the lack of adequate control in more than two-thirds of patients with
hypertension (Miller et al., 1997; JNC VI, 1997). Compliance is often defined as
implementation (by the patient) of the therapeutic plan that has been established
(Anderson et al., 1994). Nearly three-fourths of adults with hypertension are not
controlling their BP to below the recommended 140/90 mmHg (JNC VI, 1997).
Noncompliance is a multi-faceted biobehavioral issue that may be related to factors such
as economics, past history, perception of illness threat, effect illness has on daily
activities or work, presence of symptoms associated with the illness, and perception of
efficacy of therapy. Patients with chronic illnesses, especially hypertension that presents
few recognizable symptoms if any, often have difficulty prescribing meaning to their
illness. Therefore, these patients have problems complying with their therapeutic plans
(Meyer et al., 1985; McLane et al., 1995). If patients with hypertension can learn to
recognize symptoms or factors that are associated with their high BP and learn to
recognize when their BP is high, their compliance with prescribed therapy and
motivation to seek or continue treatment may improve.
At the same time that hypertensives are having problems with adhering to
treatment regimens, people throughout the world are beginning to embrace an emerging
trend called "self-managed care." Self-managed care is a term used to describe the act
ofmaintaining one's own health and well-being (Strohecker, 1999). Individuals today are
looking to manage their own health by becoming empowered and being vigilant
healthcare consumers. Because of the recommendation by the Healthy People 2010
campaign to improve patients' awareness of their BP levels and to improve the
percentage of people who know if their BP level is low, normal, or high, it is clear that it
would be beneficial for patients to have increased knowledge of their BP levels and
factors associated with their high BP. With this in mind, it makes sense that the major
health care organizations and programs are encouraging patients to have increased
awareness of BP levels and to use automatic home BP monitors to assist in the
management of hypertension (AHA, 2003a; Healthy People 2010, 2003; JNC VI, 1997).
Educational level has an impact on health and health outcomes, as educated people have
been shown to be healthier and have more improved outcomes to treatments, whereas
people of lower socioeconomic status tend to have more adverse risk factors and worse
health (Winkleby, Fortmann, & Barrett, 1990). It seems reasonable that if patients were
more aware of their high BP episodes and factors associated with them, they would be
more motivated to seek and/or continue treatment (Meyer et al., 1985; McLane et al.,
1995). Additionally, learning to recognize high BP may provide a means to teach patients
to use relaxation, biofeedback, and/or pharmacologic therapies as a means of reducing
elevated BP levels, thereby improving treatment outcomes.
Medications, known as "antihypertensive medications," are available to treat
chronic high BP. There are various types and classes of antihypertensive medications.
Each type of medication works at a different site of action in the body to lower BP. Each
medication has potential side effects that may occur with use of the medication. Often,
antihypertensives are used alone or in conjunction with other antihypertensive
medications. Because of the complex nature of hypertension, often two or more drugs or
therapies are needed to control BP to a normal level. The JNC VI report on Prevention,
Detection, Evaluation and Treatment of High BP recommends that a diuretic and/or beta
blocker be chosen as initial therapy for hypertension, unless there are specific
contraindications or reasons to choose otherwise (JNC VI, 1997).
Diuretics are a type of medication used to treat hypertension and a variety of
other illnesses that work by acting to increase urine output, thereby decreasing BP.
Diuretics inhibit sodium reabsorption and affect electrolyte excretion in a particular
nephron segment. Different classes of diuretics are available and they are generally
classified based on their major site of action within the nephron. Depending on the
diuretic class, major sites of action include the proximal tubule, thick ascending limb of
the loop of Henle, early distal tubule, and late distal and early collecting tubule. Classes
of diuretics include proximal tubule diuretics (Acetazolamide), loop diuretics
(Furosemide), thiazide diuretics (Hydrochlorothiazide), potassium-sparing diuretics
(Spironolatctone), and osmotic diuretics. Diuretics are generally well tolerated and side
effects are minimal; however, care should be taken to avoid electrolyte imbalances.
Diuretics are frequently used alone or in combination with other antihypertensive
medications for the treatment of hypertension (Smith & Reynard, 1995).
Calcium channel blockers (CCBs) are another type of medication that are used to
treat hypertension. CCBs block the movement of calcium into the arteriolar smooth
muscle and cardiac cells and may inhibit the mobilization of calcium within these cells.
In the treatment of hypertension, CCBs act as arteriolar dilators and reduce systemic
vascular resistance. CCBs are effective as monotherapy and in conjunction with other
antihypertensive medications, especially beta-blockers and central sympatholytics (Smith
& Reynard, 1995).
Beta blockers (BB) are also very effective in lowering BP in hypertension. BBs
are competitive antagonists for norepinephrine and epinephrine receptor sites in the heart,
bronchioles, and blood vessels in the skeletal muscles. The mechanism of BB action is
accomplished by blocking the beta receptors in the heart, bronchioles, and blood vessels
in skeletal muscle, and promoting vasodilation and decreasing BP. BBs decrease cardiac
output, central sympathetic output, presynaptic beta receptor inhibition, and inhibition of
renin. Different types of BBs are classified according to their site of action and
selectivity of beta receptor sites. Beta-1 selective acting agents are selective for beta
receptor sites in the heart. For example, two agents that are relatively cardio-selective
include Metoprolol and Atenolol (Smith & Reynard, 1995).
Another type of antihypertensive medication is the angiotensin-converting
enzyme inhibitors (AI). AIs are generally well tolerated and the most common adverse
effect is chronic cough. The mechanism of action of AIs is on the Renin-Angiotensin-
Aldosterone System (RAAS). Briefly, the RAAS is a key player in the regulation of
human BP. Renin is an enzyme that is found in the kidney and responds to a drop in BP,
stimulation of the SNS, or decreased extracellular sodium concentration. Renin is the
catalyst for the conversion of angiotensin I to potent, vasoconstricting, angiotensin II.
Angiotensin I is converted to angiotensin II by an enzyme found in the lung, angiotensin-
converting enzyme. The system assists the body in maintaining BP. In hypertension,
where there may be abnormally high levels of SNS activity or abnormal renin activity,
AIs work to disrupt the conversion of angiotensin I to angiotensin II (Porth, 1998).
Types of AIs include Captopril, Enalapril, Fosinopril, Rimipril, Quinapril, and Benzepril
(Smith & Reynard, 1995).
Biosituational Factors Associated with High BP
Alterations and/or uncompensated increases in SNS activity in hypertensives may
cause physical signs and symptoms. As described, increased SNS activity and
hypertension are often characterized by an increased heart rate, cardiac output, and renal
vascular resistance. These effects increase BP, flush the skin, increase fatigue, increase
heart rate, and a cause a "pounding or racing" heart (Seeley et al., 1998).
The SNS also promotes numerous metabolic effects throughout the body. These
effects include: enhanced metabolic rate of body cells, increases in blood glucose levels,
mobilization of fats to be used as fuels, and increased mental alertness via stimulation of
the reticular activating system (RAS) of the brain stem. Additionally, increased SNS
activity may promote smooth muscle cell growth and increase the likelihood of
atherosclerotic lesions and the development and/or acceleration of hypertension (Grassi
et al., 2000).
A number have studies suggest that both normotensives and hypertensives have
symptoms associated with fluctuations in their BP levels (Dimenas et al., 1989;
Pennebaker et al., 1982). In a study by Pennebaker et al. (1982), young, normotensive
subjects were evaluated to see if symptoms correlated with fluctuations in BP. Within
subject analysis found that 77% of the subjects had at least one significant symptom-SBP
correlation. Interestingly, the within-subject correlation varied from subject to subject,
indicating that different people perceive different symptoms during fluctuations in BP.
Despite the individual variations, however, symptoms of heavy breathing, pounding
heart, and fast pulse tended to be high for the majority of subjects. In contrast, another
study reported that hypertensive subjects experienced more emotional distress and
cardiac and respiratory symptoms (i.e., sweating, flushing, dry mouth, coughing,
dizziness, and dyspnea) (Dimenas et al., 1989).
BP is labile and normally fluctuates in response to both behavioral and
biosituational factors. These include activity level, posture, emotional state,
communication pattern, bodily function, and internal or external environment. People
with hypertension display significantly greater 24-hour variations in mean arterial
pressure than do normotensives (Mancia, Di Rienzo, & Parati, 1993). In our laboratory,
for example, the range of SBP of 10 hypertensive subjects varied from a minimum range
of 19 mmHg to a maximum of 56 mmHg. BP variability is influenced by both
biosituational and behavioral factors, presumably through central modulation of
autonomic drive to the heart and sympathetic blood vessels. This may be due to greater
pressor responses to emotional and other behavioral stimuli due to an increased central
emotional reactivity in essential hypertensives (Esler, 2000).
Factors such as dietary intake, gender, ethnicity, alcohol/caffeine intake, stressors,
seasonal variations, circadian fluctuations, cocaine and similar drug use, tobacco use, or
others may effect BP fluctuations (Campbell, McKay, Chockalingam, & Fodor, 1994;
Gellman et al., 1990). Brondolo et al. (1999) noted similar findings when they
investigated the effects of workday communication patterns on physiologic parameters.
It was found that naturally occurring interpersonal interactions were associated with
increases in SBP and heart rate.
Several studies have assessed whether or not the symptom "headache" was
related to BP levels. Kruszewski, Bieniaszewski, Neubause, and Krupa-Wojciechowski
(2000) reported that although 30% of stage 1 and2 hypertensive subjects (N = 150)
experienced headache during 24-hour ABPM, headache was not associated with BP
elevations, mean BP levels were not significantly higher than those during headache-free
periods, BP means 1 hour before and 1 hour after the headache were not significantly
different, and in the majority of hypertensives, the maximal BP values were recorded
outside the headache periods. Dimenas et al. (1989) similarly reported that hypertensive
subjects did not complain of headaches, as compared to other studies which show that
headache is more frequent in patients with hypertension (Bulpitt, Dollery, & Came,
1976). Headache has been speculated to be related to increased pressure and stretching
of the vessels of the dura at the base of the brain (Seeley et al., 1998).
Mood has been reported to be associated with BP. Positive mood accounted for
6% of the within subject variance for systolic and diastolic BPs (Gellman et al., 1990).
Negative mood accounted for 8% of the within subject variance for systolic and diastolic
BPs. The BPs were generally higher during the positive and negative mood states and
were lowest during a neutral mood state. Mood was classified into three categories: (a)
neutral mood (i.e., content); (b) negative mood (i.e., tense, annoyed, upset, angry); and
(c) positive mood (happy and smiling). In previous studies, it was reported that primarily
negative mood was associated with increases in BP (Brondolo, Karlin, Alexander,
Borrow, & Schwartz, 1999; James, Yee, Harshfield, Blank, & Pickering, 1986).
Communication patterns have also been associated with increases in BP.
Brondolo et al., (1999) reported that interacting with the public, supervisor, or coworker
within the prior 15 minutes of BP measurement had an stimulatory effect on BP and
cardiovascular reactivity in normotensives and hypertensives. Elevated BP responses to
positive or negative mood or communication patterns may elicit a cardiovascular
response, similar to the defense reaction hypothesis proposed by Folkow (1982).
Anger, Hostility, Stress, and Anxiety
Durel, Carver, Spitzer, Llabre, Weintraub, and Saab (1989) examined BP levels
and dispositional anger and hostility in 135 African Americans and Caucasion male and
female normotensives and unmedicated mild to moderate hypertensives. Using ABPM,
this study revealed that cognitive anger and state-trait anxiety were strongly associated
with higher SBP and DBP levels at work. In this study, women showed significant
positive relationships between hostility, anger, and anxiety and elevated BP at work.
Male subjects showed no association between anger measures and ABPM levels.
Shapiro, Goldstein, and Jamner (1996) examined the association between cynical
hostility, anger, defensiveness, and anxiety on BP in African American and Caucasion
college students. This study reported that high-hostile African American subjects had
higher SBP during the day and at night compared to high or low hostility Caucasion
subjects. African American subjects who scored high on both anxiety and defensiveness
had higher waking DBP. These studies suggest that there is an association between anger
and hostility and higher BP levels. Additionally, these studies suggest that gender,
ethnicity, type of self-report instrument, activity, and other personality traits may
influence the association (Carels et al., 1998). Factors such as anger and stress have been
shown to effect the "fight or flight" response, thereby increasing catecholamine release
and subsequent SNS effects (Seeley et al., 1998).
A stressful home environment can cause elevations in BP similar to those seen in
the work environment (Blumenthal, Towner, Thyrum, & Seigel, 1995; Carels et al.,
1998). Blumenthal et al. (1995) reported that married women had significantly higher
BP levels than unmarried women, but married and unmarried men had similar pressures.
In a study by Schnall et al. (1992), 262 employed males were studied and it was found
that social support did not affect BP independently, but the association of job strain with
DBP was stronger for the subjects who had low levels of social support.
Mild hypertensive subjects have also been shown to have greater home versus
work differences in BP, as compared to normotensives (Durel et al., 1989; Gellman et al.,
1990). Additionally, Durel et al. (1989) found that there was a significant correlation
among Caucasion and African American women between work related hostility and
anger and BP. This finding may be related to increased or augmented SNS activity in
response to stressors seen in patients with hypertension.
Work characteristics, such as perceived psychological job demands and decision
latitude, may contribute to work-related stress. Job strain is defined as "a combination of
high psychological demands together with low decision latitude." At least 12 studies
have examined job strain and ABPM in a naturalistic environment (Carels et al., 1998).
Theorell, Perski, Akerstedt, Sigala, Ahlberg-Hulten, and Svensson (1988) examined 73
normotensive men and women in six different occupations and found increased SBP
during work hours among those reporting high job strain, relative to those reporting low
job strain. Other studies examined hypertensive and normotensive subjects and
discovered that job strain was related to increased SBP and DBP at work, home, and
during sleep (Schnall, Schwartz, Landsbergis, Warren, & Pickering, 1992; Vrijkotte, van
Dooren, & de Geus, 2000). Elevations of BP at home, work, or stressful job
environments may be related to activation of the SNS and the "fight or flight" response
(Brondolo et al., 1999).
Various postural positions effect BP levels. For example, in a study performed on
87 normotensive and 44 hypertensive subjects, the effects of posture on BP were
examined. It was found that 33% to 47% of the within-subject variance in SBP and DBP
could be explained by changes in posture. As subjects in this study went from lying
down to sitting to standing, their BP systematically increased (Gellman et al., 1990). The
baroreflex mechanism is a possible physiological mechanism for changes seen through
the effects of posture. This reflex is initiated by pressure-sensitive receptors, located in
the walls of the large arteries of the neck and thoracic regions, carotid artery, and the
aortic arch. The baroreceptors respond rapidly to acute drops or elevations in BP. Upon
standing, gravitational forces push blood downward and blood flow rapidly decreases
from the head and neck regions. Baroreflex stretch receptors sense changes in
pressure/stretch and react, causing a rapid increase in action potentials toward the
cardioregulatory center in the medulla to increase pressure.
BP levels are profoundly influenced by physical activity levels. Acute physical
activity and/or exercise increase BP levels (Carels et al., 1998). Over an extended period
of habitual exercise, subjects have improved their cardiorespiratory endurance and
eventually lower resting BP and control hypertension (Jessup, Lowenthal, Pollock, &
Turner, 1998). Physical activity acutely raises BP due to the increased aerobic activity,
which increases oxygen demand, blood flow, cardiac output, and BP (Seeley et al.,
Lifestyle Factors: Smoking, Caffeine, and Sodium Intake
Laboratory studies suggest that smoking a cigarette results in an immediate and
marked increase in BP. In addition, studies have shown that ABP is higher throughout
the day in smokers compared to nonsmokers (Groppelli, Giorgi, Omboni, Parati, &
Mancia, 1992), particularly for those smokers who have consumed caffeinated beverages
(Narkiewicz et al., 1995). Smokers also tend to have much more BP variability than do
nonsmokers. Caffeine increases BP levels and potentiates cardiovascular and
neuroendocrine effects of stress in both habitual and light consumers (Lane, Adcock,
Williams, & Kuhn, 1990). Hypertensive subjects, in contrast to normotensives,
displayed significant increases in SBP and DBP after consumption of coffee. This is due
to the vasoconstricive properties of the drug caffeine (Hartely et al., 2000; Rakic, Burke,
& Beilin, 1999). A review of literature on sodium intake and BP reported that higher
intake of sodium is associated with higher BP levels. This response may be due to the
physiological water-conserving effects of sodium, thereby increasing blood volume and
BP (Chobanian & Hill, 2000).
Type A Personality
The Type A individual is characterized by feelings of time urgency, impatience,
hostility, aggressiveness, and competitiveness. The Type A personality has been
associated with increased risk of coronary heart disease. Type A individuals exhibit
higher cardiovascular responses in the natural environment, but only under certain
circumstances (i.e., stressful situation, job strain). Type A individuals have higher heart
rates and BP levels and greater BP variability than Type B individuals (Carel et al., 1998;
Steptoe, 2000). This response is most likely related to Type A individuals having
increased reactivity of the SNS and therefore continual "defense reactions."
In summary, BP is affected by numerous biological, situational, and behavioral
factors. Research studies have shown relationships between these factors and BP
variablity (Brondolo et al., 1999; Carels et al., 1988; Durel et al., 1989; Gellman et al.,
1990; James et al., 1986; Lane et al., 1990; Theorell et al., 1988). Despite the growing
research literature on relationships between biosituational or behavioral factors and
higher BP levels, it is widely held that high BP is a relatively asymptomatic event.
BP Awareness and Estimation
Discrimination of physiological processes has been of interest to researchers for
some time. Laboratory procedures have been developed to assess a subject's accuracy of
physiological parameters. Discrimination of heart rate, BP, skeletal muscle tension, and
blood glucose (Barr et al., 1988; Greenstadt et al., 1986) has been reported.
Discrimination of BP by hypertensive patients is of interest to researchers and clinicians
because hypertension is considered a relatively "silent" disease in which immediate
sensory consequences are not available to the individual. The development of procedures
that facilitate detection of BP changes may be useful in the management of hypertension.
According to Cinciripini, Epstein, and Martin (1979), techniques used to facilitate BP
discrimination should utilize procedures that are easily applied in the natural
environment and not too disruptive to the patient's lifestyle.
In the clinical setting, patients with high BP often report that they can identify
when their BP is higher then normal. Often these patients are correct in their awareness
and it has led them to receive treatment based on their physiological measurements after
subjective reporting. Patients often provide clues to their high BP through such
statements as, I just don't feel right," "I feel pulsing or throbbing in my head," or "I
feel hot and tense." While it seems clear that some people are better at sensing high BP,
the question remains as to why some people are able to do this while others are not. One
potential hypothesis is that patients with high BP have a higher SNS output and are aware
of symptoms relating to this physiologic phenomenon. While there is no direct link
between BP estimation and SNS activity, there are studies that show elevated SNS
neurotransmitters in patients with high BP (Rahn et al., 1999).
Individuals, both normotensive and hypertensive, may estimate their BP levels by
using both internal sensory and external situational information (Barr et al., 1988).
Estimations and beliefs about BP levels may or may not be accurate, but they are
important because people act upon them. In fact, Pennebaker et al. (1982) suggest that
variations in BP are correlated with different symptoms and that a person can monitor his
or her BP by monitoring symptoms. In studies where both normotensive and
hypertensive people were asked to estimate their BP levels, estimated BP was strongly
associated with symptoms and moods (Baumann & Leventhal, 1985) and with feelings of
physical tenseness and physical activity (Fahrenberg et al., 1995).
Several studies tested whether or not people can accurately estimate their BP.
The findings have been fraught with much speculation and conflicting results (Barr et al.,
1988; Baumann & Leventhal, 1985; Brondolo et al., 1999; Cinciripini et al., 1979;
Fahrenberg et al., 1995; Greenstadt et al., 1986; Luborsky et al., 1976). An important
variable among these studies was the addition of a feedback intervention.
Clinical Relevance of BP Awareness and Estimation
The question of what is a good level of accuracy in estimating BP has not
necessarily been answered with a definitive number. However, several studies examine
BP and coronary event outcomes. For example, studies assessing the effects of BP
reduction and outcomes found significant associations between relatively small
reductions in usual BP (5, 7.5, and 10 mmHg) and 34%, 46%, and 56% less stoke and at
least 21%, 29%, 37% less coronary heart disease (MacMahon et al., 1990). Therefore,
even incremental changes or awareness in BP may be a good outcome of BP estimation
research. Additionally, several studies have found that awareness of BP level is a
predictor of health outcomes in patients with hypertension (Asai et al., 2001; Hyman &
Pavlik, 2001). Therefore, it is clinically important for patients to be more aware of their
health status and BP.
BP Estimation Without a Feedback Intervention
Only two studies address the question "Can people estimate their BP without any
type of feedback or training intervention?" Table 2-1 describes the sample descriptions,
methods, and findings of each study. In both studies, subjects were generally and
statistically inaccurate in estimating their BP correctly. Interestingly, perceived BP was
associated with symptoms and moods, rather than with actual BP in a majority of
subjects. Although some participants were better estimators than others, no differences
among subject characteristics were found (Baumann & Leventhal, 1985; Fahrenberg et
Fahrenberg and his colleagues (1995) assessed whether subjects' estimation of
BP was related to various self-assessments (feeling tense, physical activity, feeling
nervous) or actual BP or heart rate. This research inquiry involved 51 hypertensive
(defined by WHO criteria) male subjects, ages 22 to 60 years and a second group of 30
volunteer hypotensive or normotensive student subjects ages 20 to 28 years. The
hypertensive group was enrolled in a rehabilitation center and was simultaneously
receiving exercise therapy, health education, group therapy, and relaxation training. The
hypertensive group participated in 3 days of psychological and physiologic monitoring.
The first 2 days were consecutive and the 3rd day was approximately 14 days after the
first days. The normotensive/ hypotensive group participated using a SpaceLabs 90207
ambulatory BP monitor (SpaceLabs, Inc, Redmond, WA). Personality assessments and
self-evaluations of physical symptoms were also collected. A programmable pocket
computer (Casio PB 1000) was used by both groups to estimate their SBP (in mmHg)
and record self-report items.
Table 2-1. Research studies: BP estimation without feedback
Authors Sample description Methods Findings
Fahrenberg, 51 hypertensive BP measured every 30 Estimated BP & actual
Franck, males & 30 minutes about 25 times; SBP were poorly
Baas, & Jost normotensive male concurrent diary of correlated; Self-ratings
(1995) and female estimated BP, physical tense & activity were
students. activity, & subjective significantly related to
states. estimated BP.
Baumann & 20 hypertensive & BP measured 2 times per Estimated BP & actual
Leventhal 24 normotensive day for 10 days. BP SBP were poorly
(1985) male & female estimated categorically correlated; 6 out of 41
subjects. (same, higher, or lower subjects had
than usual) & assessed significant correlations
moods/ symptoms. between SBP &
Estimated BP related
Within-subject correlations revealed that estimated BP was not related to actual
BP. More extended experience in BP estimation tasks did not enhance the correlation
coefficients in hypertensive patients (day 2, r = 0.32 and day 3, r = 0.27). Estimated SBP
was related to self-reports of symptoms and activity. Stepwise regression indicated that
self-ratings of tenseness and heart rate predicted estimated SBP in hypertensive patients;
however, actual SBP was not related to estimated SBP in any of the regression models.
It is unclear whether subjects had variability in their estimations or actual BP and
how often their BP was higher than 140 mmHg (normal BP cut-off point) (JNC VI,
1997). This issue is important because there may be no physiological cues for the patient
to refer to if there are not any higher than normal readings. Differences among the
hypertensive and student groups may have occurred because of differing settings (i.e.,
rehabilitation center versus naturalistic environment) and treatments (i.e., rehabilitation
environment versus no additional training). Although the findings present insight into
awareness of BP, it is premature to generalize these findings to cohorts of either
hypertensive or normotensive subjects because of the presence of potential confounding
variables and differences among groups (e.g., geographic, treatment, instrument).
Baumann and Leventhal (1985) performed a similar study that assessed three
main research questions: (a) whether moods or symptoms are associated with BP in the
work setting, (b) whether people are accurate in assessing their BP levels, and
(c) whether there are dispositional factors that are associated with people's ability to
predict elevated BP. They used a convenience sample and included a heterogeneous
group of 44 insurance company employees (20 subjects with hypertension, 24 subjects
without hypertension). The subjects' actual BP levels were measured two times per day
(in the morning and in the afternoon) for 10 days. The actual BPs were measured using a
mercury column Baumanonometer and a single tube stethoscope. There were six
experimenters who were trained as screener technicians by the Wisconsin Heart
Association. Collected data included the following:
* Actual BP.
* Estimated BP level (i.e., categorical variable-higher than usual, same as usual,
lower than usual).
* Moods/symptoms (i.e., 10-item mood list and a 12-item symptom list regarding
how the subject felt within the last hour).
* Personality measures (i.e., self-esteem scale, private-body consciousness scale).
* BP estimation confidence rating (i.e., 1 = guess, 2 = confident, 3 = very
* Initial interview questionnaire and poststudy questionnaire (i.e., questions
pertaining to whether subjects can tell if BP is up or down).
Baumann and Leventhal (1985) found that only 6 out of 41 (15%) correlations of
actual to predicted BP were statistically significant (p = 0.01) with an accuracy
correlation "r" of greater than 0.14. It was not clear how the researchers computed the
numerical estimated BP levels, as estimated BP in this study was a categorical variable
(i.e., higher, same, or lower). The results also show that BP predictions and symptoms
were correlated more strongly (56% at p = 0.05) than actual BP to predicted BP (15% at
p = 0.05). Interestingly, subjects claimed to be fairly confident in the BP predictions,
with a mean confidence rating of 2.38 out of a possible 3.
In summary, both studies found that people are generally inaccurate in estimating
their BP. Additionally, both studies reported that people estimate their BP higher when
they are experiencing symptoms that they associate with high BP. These studies provide
a glimpse into the question of whether people are aware of their BP.
BP Estimation With a Feedback Intervention
Other studies have been undertaken to answer the questions "Are people accurate
in judging their SBP?" and "Does feedback improve estimation?" Table 2-2 describes
studies that examined BP estimation and provided subjects some type of feedback
Table 2-2. Research studies: BP estimation with feedback
Author Sample Design/methods Findings
21 male & female
subjects, 9 of
male & female
Five sessions of
feedback/no feedback, 2
BP measured twice daily
for 20 days/4 weeks. 2
randomly assigned groups
received either feedback
Experiment #1: 4 sessions
(1 pre, 1 post, 2 feedback
Experiment #2: 2
sessions (1 feedback, 1 no
Experiment #3: single
session of feedback of
Experimental design with
random assignment to 4
treatment groups (no
Estimated SBP &
Estimated BP & recorded
average of 7.5 times.
Subjects provided prior
feedback from 11.5
mmHg to 7.4
was maintained over
& effects were
estimation of SBP.
Initial feedback did
of BP estimations.
estimation of DBP.
43.8% of subjects
actual & estimated
SBP after the
with 26.6% before
of actual to
Luborsky et al. (1976) performed a study on 21 subjects (16 normotensives, 5
stage-1 hypertensives) to assess the ability of people to estimate their SBP after being
given feedback of daily BP information. In this study, mean raw error (absolute value)
scores for numerical SBP were compared between baseline and feedback groups.
Feedback, in the form of providing the subject their mean previous SBP readings,
improved the estimation of SBP by 5 mmHg. The authors concluded that the key to
becoming more accurate in estimating SBP is learning your individual range of BP
Cinciripini and colleagues (1979) studied 18 normotensive student volunteers to
assess the effects of providing BP feedback on the ability to discriminate systolic and
diastolic BP. The subjects were randomly assigned to two groups, one that provided
feedback and one that provided feedback after an extended baseline period. Group 1
consisted of feedback (i.e., the mean of two BP readings for that session) that was
provided to the subjects for five days in a multiple baseline fashion. The procedure
began with an initial screening for BP variability, 5 days of baseline (no feedback), 5
days of feedback, and 10 days postbaseline (no feedback). Group 2 subjects had an
extended baseline period followed by a feedback condition. The subjects were asked to
estimate their systolic and diastolic BP levels twice a day for 20 consecutive days prior to
measuring them using a mercury sphygmomanometer. This study evaluated the
difference between estimated and actual BP using the absolute deviation in mmHg
between the estimate and actual mean daily BP. Those in group 1 improved their ability
to estimate their actual BP after the sequential implementation of feedback. The mean
SBP daily deviation score at baseline for group 1 was 9.6 mmHg and after feedback it
declined to 5.9 mmHg. This improvement continued after the feedback sessions and was
maintained during the no feedback, postbaseline period. Those in group 2 showed no
statistically significant improvement during the extended baseline period; however, their
accuracy level improved after the addition of feedback during the last week of training.
These subjects improved from a mean SBP daily deviation score of 9.0 mmHg to a score
of 3.6 mmHg after feedback was provided (Cinciripini et al., 1979).
Greenstadt and colleagues (1986) performed an experimental study on 72 healthy
normotensive volunteers to assess the benefit of discrimination training on the ability of
normotensive subjects to detect changing levels of their own BP. Overall, this study
concluded that normotensive subjects have relatively no awareness of small BP
variations, but that feedback in the form of "knowledge of results" improves BP
Barr et al. (1988) studied 64 normotensive subjects for 3 sessions (3 months
apart) to assess the effects of internal and environmental feedback on SBP estimation.
This study was unique in that it utilized biosituational feedback methods. Biosituational
feedback involves providing feedback to the patient regarding internal (e.g., actual BP,
symptoms, moods) and external (e.g., environment, posture, diet) factors that occur
during the measurement of BP (Barr et al., 1988). In the feedback phase of the study,
subjects were randomly assigned to one of four groups: no feedback, symptoms/mood
feedback, situational/activity feedback, or biosituational feedback (a combination of the
previous two feedback types). Approximately 71.4% of the subjects in the biosituational
feedback group had significant accuracy correlations, compared with 31.3% in the
symptoms/moods group, 44.4% in the situational group, and 31.3% in the control (no
Brondolo et al. (1999) provided 54 mildly-hypertensive subjects with their SBP
range after a baseline period. This study found significant within-subject associations of
actual to predicted SBP (p = 0.002) and DBP (p = 0.02) in 54 mildly hypertensive male
subjects. The authors also took into consideration factors that may influence judgments
about BP estimation including home BP monitoring and use of medications. The
findings indicate that, given some information about their previous BP, subjects display a
limited but reliable relationship between their actual and estimated SBP.
In summary, five studies that have provided feedback to people to improve their
ability to estimate their BP have shown an improvement in BP discrimination after
feedback. Different types of feedback have been used to assist subjects in learning to
recognize symptoms, situations, and factors that are associated with their BP levels.
Providing normotensive (Barr et al., 1988; Cinciripini et al., 1979; Greenstadt et al.,
1986) and hypertensive subjects (Brondolo et al., 1999; Luborsky et al., 1976)
knowledge of their actual BP levels has been somewhat successful in improving the
accuracy of BP estimation.
Discussion of BP Estimation Studies
Among the feedback intervention-type studies, all showed an improvement in BP
discrimination after feedback (Barr et al., 1988; Brondolo et al., 1999; Cinciripini et al.,
1979; Greenstadt et al., 1986; Luborsky et al., 1976). In contrast, both studies that did
not provide feedback failed to show associations between actual and estimated BP levels
(Baumann & Leventhal, 1985; Fahrenberg et al., 1995). However, both studies found
relationships between estimated BP and self-reports of physical symptoms and subjective
state. Limitations for generalizability include the use of normotensive, young-student, or
convenience samples; the amount and frequency of the feedback interventions and/or BP
estimations; and the lack of application to real-life situations and circumstances of
American hypertensive patients. If patients can be trained to recognize when their BP is
elevated, they may be candidates for some further intervention (e.g., biofeedback
training) to help control their BP. However, more research is needed to conclusively
state that patients with hypertension are either accurate or inaccurate in estimating their
This review of research provides support for using feedback methods to improve
the ability to estimate BP and suggests that BP awareness may be improved in some
people using feedback methods. The limited number of studies studying hypertensive
persons with high BP suggests that more research is needed to further assess the effects
of BP awareness feedback training among this group. Research is needed to evaluate
clinical outcomes of BP awareness training, such as BP control, patient motivation and
compliance, cost-effectiveness, and morbidity and mortality.
Over the past several years, changes have occurred in health care that have made
patients more than mere passive participants of their healthcare. Patients are much more
willing and able to learn more about their health and well-being than previous
generations (Strohecker, 1999). Teaching people about their BP and BP patterns is an
effective way to improve health of patients and empower people with hypertension to
have more control over their own life and health (Healthy People 2010, 2003). This
review of literature suggests that BP feedback interventions may be an effective means to
teach people how to learn more about their BP patterns and when their BP is elevated.
While this research is promising, more inquiry is needed to decide if training patients
with hypertension can improve their awareness of their high BP episodes and if this
training will ultimately improve healthcare outcomes.
Educational Level and Health Disparities
Major disparities exist among population groups, with a disproportionate burden
of death and disability from cardiovascular disease in minority and lower socioeconomic
populations. Health disparities are defined as differences in the incidence, prevalence,
mortality, and burden of diseases and other adverse health conditions that exist among
specific population groups in the United States. Several research studies have reported
that higher educated people tend to be healthier and have improved outcomes to
treatments, whereas people of lower socioeconomic status tend to have more adverse risk
factors and poorer health (Myllykangas, Pekkanen, Haukkala, Vahtera, & Salomaa, 1995;
Winkleby et al., 1990; Winkleby, Jatulis, Frank, & Fortmann, 1992). For example, data
from the NHANES III study showed that there were highly significant differences in BP,
body mass index (BMI), and physical inactivity for both African- and Mexican-American
women compared to white women when educational level and ethnicity were adjusted
for (Winkleby, Kremer, Ahn, & Varady, 1998). Disparities also exist in the prevalence
of risk factors for cardiovascular disease. Lower educated persons and racial and ethnic
minorities have higher rates of hypertension, BMI, physical inactivity, and non-HDL
cholesterol, tend to develop hypertension at an earlier age, and are less likely to undergo
treatment to control their high BP (NIH Online, 2003). In a study by Goldman and
Smith (2002) differences in treatment adherence by education level are examined in
patients with HIV and diabetes. It was found that patients with higher socioeconomic
status and higher educational levels had improved treatment adherence and outcomes. In
this study, the more-educated patients were more likely to adhere to therapy and have
better self-reported general health. The less-educated patients were more likely to switch
treatments, which led to worsening general health. The authors assert that the large
differences in health outcomes exist, not solely because of poor access to care or poor
health behaviors, but because of differences in educational level (Goldman & Smith,
Ambulatory BP Monitoring
Ambulatory BP monitoring (ABPM) is a naturalistic BP measurement technique
that has been evolving over the past 30 years. It is a method that allows a clinician,
patient or researcher to monitor multiple BP readings over a 24- to 48-hour period.
These devices can measure BP over time and introduce minimal intrusion into the
person's daily routine. ABPM is used clinically to assess and diagnose types of
hypertension, evaluate pharmacologic and/or nonpharmacologic therapies, and monitor
resistant and/or borderline hypertension.
Ambulatory BP monitoring has now become an established research tool in
clinical trials. The use of ABPM decreases threats to external validity and the potential
"white coat" effect of observers on physiological and psychological responses.
Oscillometric monitors measure SBP, mean arterial pressure (MAP), and heart rate (HR),
from which DBP, pulse pressure (PP), and average 24-hour BP, diurnal changes, BP
Load (percentage of systolic and diastolic readings greater than 140 and 90 mmHg during
the day and greater than 120 and 90 mmHg during the night), and BP variability (the
standard deviation of the average 24-hour daytime and nighttime measures) can be
calculated. Ambulatory BP measurements correlate with the extent of target organ
damage or cardiovascular risk. For example, Verdecchia (2000) reported that ambulatory
SBP, DBP, and PP were independently and directly associated with cardiovascular risk.
While the use of the ABPM is minimally intrusive to the person, it may pose
comfort issues such as annoyance from the beeping sound, weight of the ABPM device,
and bulkiness of the device. Over the past several years, improvements have been made
to the devices to make them more "user friendly" and comfortable for subjects to wear
for longer periods of time. Adherence has been shown to be enhanced following
empathetic discussion and demonstration of the device. The safety of ABPM techniques
have been established and complications are rare (NHBPEP-ABPM, 1992).
A typical, fully-automatic ABPM device is battery-driven and consists of an arm
cuff that can be programmed to inflate automatically throughout a 24- to 48-hour period.
BP is determined in the arm by detection of (a) Korotkoff sounds by one or two
piezoelectric microphones under the cuff (ausculatory method) and (b) oscillations
transmitted from the brachial artery to the cuff (oscillometric method). The Spacelabs
90207 ABPM device (Spacelabs, Inc, Redmond, WA) measures BP using the
oscillometric technique. Auscultatory and oscillometric techniques have not been
rigorously compared to each other to see if one is more preferable for ambulatory BP
monitoring. However, the auscultatory technique is more sensitive to environmental and
distracting noises, such as automobiles and large machinery. Oscillometric techniques
detect systolic and mean BP and use algorithms to calculate diastolic BP. This may be a
weakness as these algorithms are not appropriate for all subjects. Additionally,
oscillometric methods are affected by muscle artifacts and tremors generated beneath the
cuff. To avoid invalid or erroneous readings, the device should be calibrated properly
and the cuff should be fit to the subject prior to use. In short, ABPM is a mature and
clinically appropriate method for obtaining multiple, naturalistic ambulatory BP readings
over a period of 24- to 48-hours (NHBPEP-ABPM, 1992).
In summary, hypertension, specifically high SBP, continues to be a major
predictor of morbidity and mortality of people in the United States and worldwide. As
many as 50 million American people are estimated to have hypertension (AHA, 2003a).
Isolated systolic hypertension is prevalent among the elderly and people greater than 50
years of age (Franklin et al., 2001). Current diagnostic and treatment modalities have
been wrought with difficulties due to a variety of physiologic, psychologic, socio-
economic, and practical factors. Current research suggests that the sympathetic nervous
system plays a major role in the development and/or maintenance of hypertension
(Rumantir et al., 2000). Activation of the SNS leads to a documented
psychophysiological "fight or flight" response and associated manifestations. It is
unknown whether high BP is associated with symptoms; however the majority of current
knowledge suggests that it is an asymptomatic phenomenon. Despite the overwhelming
support that hypertension is an asymptomatic disease, studies using BP and biosituational
feedback have shown that people can be trained to become more aware of their BP
levels. It is unknown whether the combination of ambulatory BP methods and
biosituational self-awareness training improves subjects' ability to recognize when their
BP is elevated. Due to the recent surge of knowledge regarding the sympathetic nervous
system's connection with hypertension, it seems likely that some people, if not all
people, could be trained to become more aware of the increased SNS activity.
PROCEDURES AND METHODS
The purpose of this research was to determine if subjects with hypertension could
improve their estimation of their SBP after an ambulatory BP feedback and biosituational
self-awareness training intervention.
A prospective cohort, repeated measures, pretest/posttest design was employed
for this study. A repeated measures design allows subjects to serve as their own control
and within-subject differences to be analyzed. The design, analysis groupings, and data
measured are graphically displayed in Table 3-1.
Population and Sample
The population under investigation was adult hypertensive persons, aged 21 to 65,
in the northern Florida area. Subject recruitment was done through both flier advertising
and BP screening. The investigator offered BP screening over the course of a 12-month
period at various locations. Before BP was measured, potential subjects were told that
they would be offered the opportunity to take part in a research study if they qualified.
BP was measured twice 2 minutes apart after the subject sat quietly for 3 to 5 minutes. If
the BP measurements differed by more than 5 mmHg, an additional BP measurement
was taken. The initial BP screening was obtained by averaging the two BP readings that
agreed within 5 mmHg. Subjects who met the inclusion and not the exclusion criteria
were asked to participate in the study. Every attempt to include diverse participants
Table 3-1. Description of design, analysis groupings, and data measured
Group Hypothesi Pretraining Training Posttraining
Adult hypertensives H 1 ASBP, ESBP, ASBP, ESBP ASBP, ESBP,
(total sample) mean AD mean AD
Adult hypertensives H 2, H 3 ASBP, ESBP, ASBP, ESBP ASBP, ESBP,
college educated MI MI
Adult hypertensives H 2, H 3 ASBP, ESBP, ASBP, ESBP ASBP, ESBP,
noncollege- educated mean AD mean AD
Adult hypertensives H4 ASBP, ESBP, ASBP, ESBP ASBP, ESBP,
BMI < 30 MI MI
Adult hypertensives H4 ASBP, ESBP, ASBP, ESBP ASBP, ESBP,
BMI > 30 MI MI
Adult hypertensives H5 ASBP, ESBP, ASBP, ESBP ASBP, ESBP,
male MI MI
Adult hypertensives H5 ASBP, ESBP, ASBP, ESBP ASBP, ESBP,
female MI MI
Hypertensives < 48 H6 ASBP, ESBP, ASBP, ESBP ASBP, ESBP,
years of age MI MI
Hypertensives 48 H 6 ASBP, ESBP, ASBP, ESBP ASBP, ESBP,
years of age MI MI
Antihypertensive H7 ASBP, ESBP ASBP, ESBP ASBP, ESBP
Antihypertensive H 7 ASBP, ESBP ASBP, ESBP ASBP, ESBP
medication Users__ _
Note: ASBP represents actual SBP, ESBP represents estimated SBP, mean AD
represents mean absolute difference, and MI represents mean improvement.
(i.e., gender, race, socioeconomic, age, and ethnicity) was made. To determine the
sample size, it was estimated that subjects could improve their estimation of SBP by
decreasing the difference by half. For example, if the mean difference between the actual
and estimated SBP was 10 mmHg on day 1, this difference would drop to 5 mmHg.
Assuming that the deviation of the difference was 4.0 mmHg, setting an alpha of 0.05,
and using a 2-tailed test, 8 subjects would be required to achieve at least 80% power.
Recognizing that subjects may not be able to improve their estimation this much with
only a 2-day training period, a second determination of sample size was completed based
on an improvement of 2 mmHg, the smallest effect that would be important to detect.
Again, if on day 1 the mean difference between the actual and estimated SBP was 10
mmHg and the mean difference on day 4 was 8 mmHg, this would constitute an
improvement of 2 mmHg. Assuming a standard deviation of the difference to be 4.0
mmHg, setting an alpha of 0.05, and using a 2-tailed test, 34 subjects would be required
to achieve at least 80% power. Recognizing that these are estimates and there are no data
suggesting the appropriate effect size to use, 42 subjects were recruited for study to allow
for attrition and incomplete data.
To ensure that subjects would have adequate variability to be able to detect
differences, we randomly selected ambulatory BP data from 10 hypertensive subjects in
Dr. Yucha's research study. For these 10 subjects, the average daytime range in SBP was
33.2 mmHg, ranging from a minimum of 19 to a maximum of 56 mmHg. Therefore, we
felt confident that subjects would have adequate variability in their BP to detect
differences (unpublished BP variability data, 2001).
Inclusion and Exclusion Criteria
The specific inclusion criteria were as follows:
* men or women 21 to 65 years diagnosed with hypertension or taking
antihypertensive medications, living in the North Florida area.
* ability to come to the research office at least four times.
* ability to speak and understand English.
* able to verbally communicate with intact memory.
* ability to read English at an eighth grade level or greater.
Subjects who could respond to requests for participation were considered to have
adequate communication skills and memory ability. Subjects were excluded from the
study if their history demonstrated significant cardiovascular, renal, or psychiatric
diseases. There was no exclusion of subjects based on gender or race.
The setting for this study was a county located in Northern Florida. Initially, the
subjects were screened in the laboratory or field setting. The pretraining, training, and
posttraining sessions occurred in the subjects' natural environment during daytime hours
while the subjects were awake.
Research Variables and Instruments
Demographic Data Sheet
The demographic data sheet included information regarding age, gender, race,
marital status, how long with diagnosis of hypertension, height, weight, body mass index
(BMI), and education.
Health History Form
The health history form included yes/no type questions regarding the presence or
absence of health conditions including high BP, diabetes, heart and cerebral disease,
psychiatric disorders, and other chronic diseases. Additionally, questions regarding past
or present smoking, alcohol use, high cholesterol, exercise level, medications, and family
cardiovascular health history were included.
Ambulatory BP Monitor
Naturalistic ambulatory monitoring of BP in human subjects was preferred in this
study because it enhances the generalizability of the findings to outside of the laboratory
setting and it does not interfere with most of the subjects' usual daily activities. The
SpaceLabs ABPM (Model 90207, SpaceLabs, Inc., Redmond, WA), an automatic
noninvasive oscillometric recorder, was used to collect SBP data. This monitor measures
BP by detection of oscillations transmitted from the brachial artery to the cuff. The
monitor was equipped with four different size adult cuffs. A SpaceLabs (Model 9029,
Redmond, WA) Data Interface Unit was used for data retrieval and report generation.
The ABPM can be programmed to display the BP readings on its' LCD screen
immediately after measurement (i.e., unblinded) or not to display the BP readings (i.e.,
blinded). This feature worked well for this study, as different time periods required
"blinding" or "unblinding" of the LCD screen. The reliability of the SpaceLabs ABPM
device has been studied extensively over the last few years. Correlation coefficients
between two sets of readings have ranged between 0.72 and 0.93 for SBP, indicating that
the reliability is acceptable (Pickering et al., 1994). Pickering et al. suggest that at least
five or six readings would give an adequate representation of the average pressure in a
particular setting such as work or home. In addition, a sampling frequency of one
reading every 30 to 60 minutes has been suggested to adequately describe average SBP
levels in different settings. This instrument has a high level of accuracy and clinical
performance and meets Association for the Advancement of Medical Instrumentation
guidelines and the guidelines of the British Hypertension Society (O'Brien, Atkins, &
Staessen, 1995). Artifactual readings were eliminated using the Casadei procedure, a
standard editing criteria (Winnicki, Canali, Mormino, & Palatini, 1997). Similar to other
editing criteria, the Casadei procedure eliminates measurements that fall outside 50 to
240 mmHg for SBP, 40 to 140 mmHg for DBP, 40 to125 beats per minute for heart rate,
and 20 to 100 mmHg for pulse pressure.
Rigorous calibration of the monitor was made prior to ABP monitoring. A
calibration procedure comprised of three calibration readings taken simultaneously with a
mercury column sphygmomanometer and the ABP monitor, by means of a "T-connector"
between the two instruments. Readings for both SBP and DBP agreed within 5 mmHg of
one another on all three attempts.
For the purpose of this study, the ABPM was initialized to measure BP every 30
minutes. Actual ambulatory BP measurements were recorded as numerical continuous
response variables. After measurement of ambulatory BP, BP data were downloaded
using SpaceLabs Data Management Software (Redmond, WA) and the data.
Actual BP was a continuous variable that was measured using a SpaceLabs
Ambulatory BP Monitor (Model 90207, SpaceLabs Inc., Redmond, WA).
Estimated Systolic BP
Estimated SBP was a continuous numerical variable that was estimated by the
participant in mmHg and was based on the guideline provided to the participant.
Participants were also invited to circle the range of SBP that they thought their SBP was
in at the time of cuff inflation and BP measurement. This was done to improve the
conceptualization of the participant to estimating his/her own SBP. If range information
was the only method of estimating for the subject, the average of the range was computed
and entered as the subjects' estimation of SBP.
The absolute difference (AD) is defined as the absolute value of the mean
difference. The absolute difference was calculated for mean actual SBP day 1, mean
estimated SBP day 1, mean actual SBP day 4, and mean estimated SBP day 4.
The mean improvement is defined as the absolute value of the mean difference of
day 1 (mean actual SBP minus mean estimated SBP) minus the absolute value of the
mean difference of day 4 (mean difference of actual SBP minus estimated SBP).
Pre- and Posttraining SBP Estimation Form
The pre- and posttraining SBP Estimation Form provides subjects with a
guideline for SBP estimation that is based on the classification defined by the Joint
National Committee on Prevention, Detection, Evaluation, and Treatment of High BP
(JNC VI, 1997). This tool categorizes SBP based on the JNC VI (1997) classification
and provides categorical descriptions of each range of SBP category. This serves to help
subjects conceptualize their SBP, so that they can estimate their SBP level. Subjects are
instructed to write an estimate of what they think their SBP level is at the start of cuff
inflation. Subjects were instructed that they may circle the range of where they think
their SBP falls, if this was more understandable for the subject.
SBP Estimation Training Form and Self-Awareness Checklist
The training form is a form that is used during days 2 and 3. One form was used
for each BP measurement/estimation. The form consists of an area for the subject to
write the time of BP measurement, estimated SBP level (subject estimates), and actual
SBP level (from the monitor). The Self-Awareness Checklist is a yes/no checklist. It is
made up of 38 mood, symptoms, and situation items. This checklist has been adapted
from research on physical symptoms and factors relating to BP (Barr et al., 1988;
Brondolo et al., 1999; Gellman et al., 1990).
Demographic characteristics of subjects were examined by nine indicators:
gender, race, education, marital status, age, height, weight, body mass index, and how
long with diagnosis of hypertension.
Gender. Gender was a categorical variable coded as male or female.
Race. Race was a categorical variable coded as White, Black, Hispanic, Asian,
Education. Education was categorized into seven groups according to the number
of years of formal education which the participants completed: less than 7 years, junior
high school (grades 7-9), some high school (grades 10-11), high school graduate, some
college or technical school, college graduate, and graduate school (master's degree or
beyond). For data analysis purposes, education was further compressed into two
variables: H.S./technical school and college educated.
Marital status. Marital status was coded into one of four categories reflecting the
status of married, widowed, divorced/separated, or never married.
Age. Age was recorded as actual years and was coded into five categories
reflecting years of age: 21-30, 31-40, 41-50, 51-60, 61-65. For data analysis purposes,
age was further compressed into two categories: > 48 years of age and < 48 years of age.
Weight. Weight was a continuous numerical variable that was recorded in
Height. Height was a continuous numerical variable that was recorded in
Body Mass Index (BMI). BMI was calculated as the ratio of the weight in kg to
the square of the height in meters.
Length of time since diagnosis of hypertension. Length of time since diagnosis of
hypertension was categorized as follows: less than 5 years, 5-10 years, 11-20 years, 21
years or more.
Health Status Variables
Four indicators were utilized to identify the health status, family cardiovascular
health history, and the use of prescribed and nonprescribed medicines. These variables
included (a) existence of health problems, (b) number and type(s) of medications used
daily, (c) family cardiovascular health history, and (d) lifestyle factors. Below is a
description of these variables.
Health problems. The participant was asked to identify his or her health problems
from a list of different illnesses. The answer was coded zero when the problem did not
exist and one if the problem existed.
Use and type of medications. The use of all types of medications was a
categorical variable that was coded zero if there were no medications used and one if the
participant used medications on a daily basis. If the answer was yes, the participant was
asked to name all prescribed and nonprescribed medications that are used daily. For data
analysis purposes, the medication variable was further described to account for
differences among types of medications and antihypertensive medications. A variable
coded as "htntype" was created and was coded as 0 if they were taking no hypertensive
medications, 1 if they were using ace inhibitors, 2 if they were using calcium channel
blockers, 3 if they were using beta blockers, 4 if they were using diuretics, 5 if they were
using other antihypertensives, and 6 if they were using 2 or more antihypertensive
Family cardiovascular health history. Each participant was asked to identify
illnesses that his or her blood relatives have had or currently have. Family
cardiovascular health history was coded into five categorical variables including heart
attack, high BP, stroke, diabetes, and high cholesterol. The answer was coded zero if
there was no family history of the disease. The variable was coded 1 if there was a blood
relative with one of the identified illnesses, 2 if there were 2 identified illnesses, 3 if there
were 3 illnesses chosen, 4 if there were 4 chosen, and 5 if there were 5 illnesses chosen.
Lifestyle factors. Lifestyle factors were considered questions relating to alcohol
use, caffeine use, exercise level, and cholesterol elevation. The responses were coded
zero if the respondents chose no and one if the respondents chose yes.
Table 3-2. Instruments used and variables measured during the study periods
ABP Monitor Actual SBP
Pre-/Posttraining Form Estimated SBP
Training Form/Self-Awareness Estimated SBP
Checklist Actual SBP
Demographic Data Sheet Gender
Time with hypertension
Date of Birth
Health History Form Personal history of cardiovascular, renal,
liver, thyroid diseases, diabetes mellitus,
caffeine, alcohol and tobacco use, exercise,
medication usage, and family history.
Classification of Adult BP
The criteria for classifying BP as defined by the Joint National Committee on
Prevention, Detection, Evaluation, and Treatment of High BP (JNC VI, 1997) was used
to assist subjects to estimate their actual BP. Table 3-3 shows the classification for adult
BP as defined by the JNC VI (1997).
Table 3-3. Adult BP classification
Category Systolic BP (mmHg) Diastolic BP (mmHg)
Optimal Less than 120 and Less than 80
Normal Less than 130 and Less than 85
High-Normal 130-139 or 85-89
Stage 1 140-159 or 90-99
Stage 2 160-179 or 100-109
Stage 3 180 or greater or Greater than 110
Study Protocol and Procedures
This research consisted of three phases: (a) initial interview and pretraining
measurement and estimation of BP (one day period), (b) ABPM and biosituational self-
awareness training (2-day period) and (c) posttraining measurement and estimation of BP
After the appropriate institutional review and approval, subjects were recruited
from northern Florida. The investigator recruited participants using fliers and
advertisements that were posted near the University of Florida, the Veterans
Administration clinics, hospitals, and various public areas in the north Florida area.
Recruitment fliers were also sent to female veterans with hypertension in the northern
Florida area. Attempts to include diverse participants (i.e., gender, age, and race) were
made. Those subjects who met the inclusion criteria and who did not meet the exclusion
criteria were asked to participate in the study.
Initial Screening Procedures
The initial screening occurred in either the laboratory or field setting. The
procedure for measuring BP was in accordance with JNC VI recommendations, using the
ABPM. To assure that the ABPM readings are valid, calibration of the equipment was
performed. The investigator calibrated the ABPM using simultaneous determinations of
BP by auscultation and a mercury sphygmomanometer (using T connector) and
agreement of at least 3 sequential readings to within 5 mmHg systolic and diastolic was
found (NHBPEP-ABPM, 1992).
The BP measurement began after approximately 3 to 5 minutes of quiet rest,
sitting in a chair. The subject was seated in a chair with his/her back supported and
nondominant arm bared and supported at the heart level. The appropriate cuff size was
determined to ensure accurate measurement. The bladder within the cuff encircled
approximately 80 % of the subject's arm in accordance with JNC VI recommendations
(JNC VI, 1997). The investigator provided the subject with an initialized, programmed
and fitted ambulatory BP monitor. The investigator performed two BP measurements
approximately two minutes apart, in accordance with recommendations of the JNC VI
(1997, p. 12). If these two measures were more than 5 mmHg apart, a third measure was
taken. The average of the measurements were provided to the patient as their "average
Ambulatory BP Monitoring Protocol
The subject was instructed to refrain from excessive physical exertion and water
activities while wearing the BP monitor. The subject was instructed to keep a regular
sleep and wake pattern and to avoid any unusual physical exertion or excessive stress
during the study period. The subject was instructed that he/she could remove the monitor
for short time periods if these activities were unavoidable. Then, the subject was given
the opportunity to use and become familiar with the ABPM.
Ambulatory BP was measured on an ordinary work, home, or school day for each
subject. To ensure that the subjects were experiencing "usual" symptoms or situations,
subjects were asked prior to beginning each study day how they were feeling on that day
and if they were feeling "well" or "usual." If the subject was not feeling as he/or she
normally feels (e.g., has a cold/flu or other anomaly), the session was postponed until the
following day or a more "usual" day.
To ensure subject safety, subjects were instructed to sit, rest, and call their
primary health care provider in the event that their BP was greater than 180 mmHg
systolic or 110 mmHg diastolic over two consecutive periods. Because of the nature of
the ABPM device, subjects were instructed that they could push the "start" button on the
monitor and measure their BP in more frequent intervals than were programmed. In
addition, subjects were instructed to call their health care provider or seek emergency
care if they experienced any other serious discomforts other than the minimal
discomforts associated with the use of the ambulatory BP monitor. Subjects were
instructed that symptoms such as chest pain, shortness of breath, or numbness or tingling
of face, legs, or arms should be reported immediately to their healthcare provider.
Subjects were fitted with an ABP monitor and familiarized with its use. The
monitor was programmed to measure BP every 30 minutes over a 6-hour period.
Subjects were instructed that they could wear the monitor during their usual awake hours,
generally between the hours of 6 am and 10 pm. Each subject was fitted with a proper-
sized BP cuff, fitted according to JNC VI recommendations (JNC VI, 1997). To ensure
that the cuff was not too tight, the investigator inserted a finger between the bladder of
the cuff and the subjects' arm. Subjects were provided an ABPM tote bag or hip strap to
assist in carrying the ABP monitor.
The monitor emits a series of 5 beeps prior to measurement of BP and cuff
inflation. The subject was instructed to listen for these sounds and to hang their arm
freely at their side during cuff inflation. They were also instructed to keep the bladder of
the cuff at or near the level of their heart, to avoid measurement errors. At cuff inflation,
subjects were instructed to estimate their BP. On days 2 and 3, subjects were also
instructed to document their actual SBP as well as their moods, symptoms, and activities
during the BP measurement.
After the initial screening for inclusion/exclusion criteria, a convenient meeting
date and time to start the study was arranged. Informed consent was obtained and a copy
of the informed consent and contact information for the investigator and dissertation
chairperson was provided to each participant. Subjects were informed that participation
in this study will not change the way they are treated for high BP. The subject was
instructed to continue doing exactly what his/her doctor has prescribed. Each participant
was advised of his or her rights as a research participant and the right to decline without
penalty. The investigator arranged a time and place for the initial interview, either at the
research office or the subject's home. The investigator instructed the subject about the
study procedures and that data would be collected over a 4-day period. The participants
were notified that there was monetary compensation of $10.00 per day for each day that
After informed consent was obtained, the subject was asked to answer questions
related to demographics, health status, family history, and medication usage. The entire
interview took approximately 15-30 minutes per subject. After completion of the initial
interview, data were entered into a data spreadsheet for analysis.
When the subject was comfortable with the ABPM operation and function, the
subject started Day 1 data collection period and took the ABPM home, work and/or to
their "natural" environment. The participant was instructed to estimate numerically their
SBP using guidelines from the JNC VI (1997). The LCD screen on the ABPM was
"blinded" (i.e., no BP readings were displayed). The subject was instructed to return to
the clinic the following day with the ABPM, or arrangements for a field visit were made.
Days 2 and 3
On the second study day, day 1 data were downloaded and edited using the
SpaceLabs (Model 9029, Redmond, WA) Data Interface Unit. Data were entered into a
data spreadsheet for analysis. The ABPM was initialized and reprogrammed to display
the BP readings on the LCD screen. The subject was provided information on potential
biosituational factors that may affect BP. The subject was given the opportunity to use
and become familiar with the Training Form/Self-Awareness Checklist. The subject was
instructed to fill out the Self-Awareness Checklist at each BP reading. The subject was
instructed that SBP, DBP, and HR are visible in the LCD screen after each BP
measurement. Next, the subject was asked to look at and write down his or her actual
SBP level as it appears on the LCD screen after each reading. Subjects were instructed to
estimate their SBP in a similar fashion as in day 1, when the cuff began to inflate.
When the subject was confident with using the Self-Awareness checklist and
Training Form, he or she was instructed to wear the ABPM for two consecutive days in
the "normal" environment and perform the instructed tasks every 30 minutes for six
hours each day.
On the fourth study day, the subject and investigator met again. The data were
downloaded onto a spreadsheet for analysis. The ABPM was initialized and re-
programmed not to display the BP readings. Similar to day 1, the LCD screen was
"blinded" to the subject (i.e., the BP reading were not be visible to the subject). The
subject was instructed to think about the biosituational factors that occurred during their
SBP measurements and when SBP was high. Subjects were given an opportunity to
assess the biosituational self-awareness factors that were related to high SBPs (according
to individual responses).
Subjects were instructed to wear the ABPM monitor for 6 hours and estimate
their SBP, making decisions based on their biosituational self-awareness factors and BP
readings, during the previous 2 days.
At the conclusion of the study, subjects were instructed to return the ambulatory
BP monitor and all forms to the investigator. Subjects were thanked for their
participation and were given a printed analysis of the 4-day ABPM readings. Each
subject received $10.00 compensation for each day they completed. The subjects
received a total of $40.00 monetary compensation for participation in this study. Study
procedures are outlined in Table 3-4.
Methods of Statistical Analyses
Data were analyzed using SPSS (SPSS, Inc., Chicago, Illinois). Descriptive
statistics were computed to obtain the summary measures for the data addressing the
research hypotheses. Estimated SBP data was obtained from the pre-/posttraining SBP
Estimation Form. Actual SBP measurement data was obtained from the data recorded
using the ABP monitor and the report generated by the SpaceLabs (SpaceLabs, Inc.,
Redmond, WA) Data Interface Software. These data were entered into data files for
analysis using Microsoft Excel (Microsoft Inc.) software and SPSS (SPSS, Inc., Chicago,
Illinois) statistical software. Descriptive statistics were computed to identify the
demographic characteristics of the participants, number and types of medications used,
health problems, and family health history. Study variables (estimated and actual SBP,
absolute difference (AD) of the mean scores of day 1 and 4, and mean improvement)
were summarized and graphed across time. For data analysis purposes, day 2 and 3 were
combined and a total mean score for actual SBP, estimated SBP, and absolute difference
were calculated for the two days. Analysis concerning the relationships between actual
and estimated SBP were performed using paired-samples t-tests. For Hypothesis 1 and 3,
paired-samples t-tests were used to compare the mean improvement between day 1 and
day 4 within groups. For Hypotheses 2 and 4 through 7, independent samples t-tests
were used to compare the means between groups of subjects. See Table 3-1 for a
description of the design, analysis groupings, and data measured in this study.
Table 3-4. Procedures for SBP estimation study
Phase 1: Initial Interview and Pretraining (Day 1)
In laboratory/Field Setting:
Screen for Inclusion/Exclusion criteria
Informed Consent Process
Calibrate & initialize ABPM (BP readings not shown) and determine cuff size
Obtain demographic, health status, health and family health history, and
medication usage data
Provide basic information about SBP
Obtain "average" baseline BP and provide information to subject
Introduction to Pre-/Posttraining Estimation Form and ABPM
Allow subject to practice using SBP estimation form and ABPM
In natural setting:
Subject estimates SBP (LCD blinded) for 6 hours at start of each cuff inflation
Phase 2: Training (Days 2 & 3)
Initialize ABPM (BP readings shown)
Provide information on SBP Estimation and BSMA factors
Demonstrate ABPM and Training Form/Self-Awareness Checklist
Allow subject to practice using ABPM, BP estimation, and Self-Awareness
In natural setting:
Subject estimates SBP for 6 hours at start of cuff inflation
Complete Training Form (SBP estimation, Self-Awareness Checklist, & actual
Phase 3: Posttraining (Day 4)
Initialize ABPM (BP readings not shown)
Instruct patients to think about biosituational self-awareness factors & SBP
feedback while estimating their SBP
In natural setting:
Estimate SBP (LCD blinded) for 6 hours at start of cuff inflation
The primary purpose of this study was to determine if hypertensive persons could
learn to estimate their SBP using a BP feedback and biosituational self-awareness
training intervention. This was determined by comparing the accuracy of the SBP
estimation before and after training. The secondary purpose of this research was to
compare the differences in the mean improvement of actual to estimated SBP between
different groups of hypertensives within the sample. These groups include college-
educated (CE) hypertensives compared to non-CE (NCE) hypertensives, hypertensives
with a body mass index (BMI) < 30 compared to hypertensives with a BMI > 30, male
hypertensives compared to female hypertensives, hypertensives less than 48 years of age
compared to hypertensives > 48 years of age, and hypertensive medication (HM) users
compared to hypertensive medication (HM) nonusers.
This chapter will first present descriptive statistics, including means, standard
deviations, and frequency distributions for each variable. The hypotheses posed in
Chapter 1 will be addressed using paired samples t-tests and independent samples t-tests.
For all results, data will be expressed as means + standard deviations and/or percentages.
Over 60 potential subjects were screened for inclusion in this study. However,
only 42 subjects met the final inclusion criteria. Of these 42 subjects, 3 subjects were
excluded from the analysis for different reasons. One male subject was excluded after
completion of day 1 because his BP on day 1 was low. This subject had a mean SBP on
day one of 101 mmHg and a minimum BP of 74/52. The subject reported symptoms of
"not feeling well" and was being treated for chronic hypothyroidism. It was
recommended that the subject seek care from his healthcare provider and withdraw from
the study. A female subject was excluded from the study after day 1 because her BP
levels were excessively high. Her mean SBP level was 192 mmHg and her maximum BP
was 201/116. She was advised to obtain immediate medical care. She contacted her
physician, obtained medical treatment, and was released from the study. A third subject
withdrew from the study after day 1 because of difficulties that she had in performing the
protocol activities during her normal work/home day.
A total of 39 subjects completed the study protocol. Of the total, 15 subjects were
male and 24 subjects were female. The male group ranged from 26 to 65 years with a
mean age of 45.1 years. The female group ranged from 21 to 65 years, with a mean age
of 50.4 years.
Subject demographics expressed in numbers and percentages were gender, race,
age, marital status, family history of hypertension, veteran status, time with diagnosis,
education level, hypertension medication type, overall medication type, and habits of
cigarette smoking, alcohol use, caffeine use, and exercise. Table 4-1 shows the subject
demographics for the total hypertensive sample (N = 39), NCE subjects (N = 15), and CE
subjects (N = 24). Table 4-2 compares the lifestyle variables for the total hypertensive
sample, NCE subjects, and CE subjects. Table 4-3 compares the health status data of the
total sample of hypertensives, NCE subjects, and CE subjects.
Table 4-1. Comparison of demographic data for the total sample, college-educated
subjects, and noncollege-educated subjects
30 and under
(N = 39)
(N = 24)
Table 4-2. Comparison of lifestyle data for the total sample, college-educated subjects,
and noncollege-educated hypertensive subjects
(N = 39)
(N = 24)
Current Tobacco Use
Regular Alcohol Use
Regular Caffeine Use
Table 4-3. Comparison of health status data for the total sample, college-educated
hypertensive subjects, and noncollege-educated hypertensive subjects.
Total sample educated subjects subjects
(N = 39) (N = 24) (N = 15)
N(%) N(%) N(%)
Time with diagnosis of hypertension
Less than 5 years 27 (69.2) 14 (58.4) 13 (86.7)
5-10 years 6(15.4) 6(25.0) 0(00.0)
11-20 years 4(10.3) 2 (8.3) 2(13.3)
21 or more years 2 (5.1) 2 (8.3) 0 (0.0)
Family history of cardiovascular disease
No family history 2 (5.1) 0 (0.0) 2(13.3)
1 FH item selected 4 (10.3) 2 (8.4) 2 (13.3)
2 FH item selected 9 (23.1) 6 (25.0) 3 (20.0)
3 FH item selected 6 (15.4) 3 (12.5) 3 (20.0)
4 FH item selected 10 (25.6) 5 (20.8) 5 (33.4)
5 FH item selected 8 (20.5) 8 (33.3)* 0 (0.0)*
Hypertension medication type
Not taking HTN meds 16 (41.0) 9 (37.5) 7 (46.7)
Ace inhibitor only 8(20.5) 4(16.7) 4(26.7)
Calcium channel blocker only 3 (7.7) 3 (12.5) 0 (0.0)
Beta blocker only 2 (5.1) 0 (0.0) 2(13.3)
Diuretic Only 2 (5.1) 2 (8.3) 0 (0.0)
Other HTN med only 1 (2.6) 1 (4.2) 0 (0.0)
2 or more HTN meds 7(18.0) 5(20.8) 2(13.3)
Overall medication type
Not taking medications 6 (15.4) 3 (12.5) 3 (20.0)
Taking HTN meds only 10(25.6) 4(16.7) 6(40.0)
Taking other type of meds only 10 (25.6) 6 (25.0) 4 (26.7)
Taking other med and HTN 13 (33.4) 11 (45.8)* 2 (13.3)*
* indicates p 0.05 by Mann-Whitney-U Nonparametric Tests.
The clinical characteristics of the subjects, including age, weight, height, BMI,
actual and estimated SBP day 1, actual and estimated SBP day 2 and 3, actual and
estimated SBP day 4, mean absolute differences of actual SBP (ASBP) minus estimated
SBP (ESBP) for each day, and number of observations are expressed using means and
standard deviations and are presented in Table 4-4. The mean scores for each study day
and across all study days are summarized in Table 4-4. The mean ASBP measurements
were similar among the total sample on days 1 and the average of days 2 and 3; 137.0 +
11.0 mmHg and 136.1 + 15.3 mmHg, respectively. On day 4, the mean ASBP was
slightly lower at 136.1 + 12.1 mmHg, but this reduction was not statistically significant.
Among the 39 subjects, there were 485 BP measurements/estimations on day 1, 880 BP
measurements/estimations on day 2 and 3, and 482 BP measurements/estimations on day
4. In total, there were 1847 BP measurements/estimations among the 39 subjects for the
total 4-day study period.
Table 4-4. Clinical characteristics for the total sample (N = 39)
Total Sample (N = 39)
Initial screening Day 1 Day 2 & 3 Day 4
Age (yrs.) 48.4 + 11.5
Weight (lbs.) 194.1 + 46.3
Height (in.) 66.7 + 4.6
BMI (kg/m2) 30.5 + 5.4
Actual SBP (mmHg) 137.0 + 11.0 137.1 + 9.27 136.1 + 12.1
Mean Actual SBP Range (mmHg) 51 36 52
Min ASBP (mmHg) 94 91 99
Max ASBP (mmHg) 176 192 174
Estimated SBP (mmHg) 137.3 + 8.6 136.0 + 5.49 136.1 + 11.8
Absolute difference ASBP-ESBP (mmHg) 10.1 + 3.5 7.5 + 5.70 9.3 + 3.2
Number ofASBP-ESBP observations 12.4 + 2.3 20.9 + 6.9 12.3 + 1.7
Analytic Results for Hypotheses
Procedure for Calculating Mean Scores
As described previously, the study protocol involved 4 days of BP measurement,
at a frequency of every 30 minutes for 6-hours each day. Therefore, theoretically each
subject should have 12 observations or BP measurements/estimations per day. However,
on Day 1, the number of BP observations for each subject ranged from 9 to 20
observations, with a mean number of observations at 12.4. Likewise, on day 4 the
number of BP observations for each subject ranged from 9 to 15 observations with a
mean of 12.3 observations. This variation occurred for a number of reasons. First, some
subjects correctly had their BP taken 12 times but the BP measurement was deleted due
to an error. The error may have been caused by improper inflation/position of the cuff,
too much activity of the arm or body during cuff inflation, and/or the BP reading was
higher than the previous BP reading and the cuff did not inflate to an adequate level to
obtain the reading. Secondly, a few subjects did not follow instructions completely and
performed either too few (9 to 11) readings or too many (13 to 20) readings. The
majority of subjects performed the tasks as directed and performed 12 readings. Data
were included if there were at least 9 observations per day. All 39 subjects had at least 9
observations per day. To assure that the mean score reflected the variation in number of
observations per day, each individual subject's scores were analyzed separately to
compute a mean actual SBP, mean estimated SBP, and a mean absolute difference
between actual and estimated SBP for each subject.
Absolute difference. The absolute difference (AD) is defined as the absolute
value of the mean difference. Without using absolute difference, overestimates and
underestimates would average to a smaller mean difference. The absolute difference has
been calculated for day 1 (mean actual SBP minus estimated SBP day 1), day 2 and 3
(mean actual SBP minus estimated SBP day 2 and 3 combined), and day 4 (mean actual
SBP minus estimated SBP day 4).
Mean improvement. The mean improvement is defined as the absolute value of
the mean difference of day 1 (mean actual SBP minus mean estimated SBP) minus the
absolute value of the mean difference of day 4 (mean difference of actual SBP minus
estimated SBP). The mean improvement represents a measure of improvement in SBP
estimation between day 1 and day 4.
The Paired Sample t-Test
The paired sample t-test was used to compare the means of two scores from
related samples. The assumptions of a paired t-test are that the variables are at interval or
ratio levels and that they should be normally distributed. Figure 4-1 depicts the
improvement scores of the entire sample of adult hypertensives. It illustrates a relatively
normal distribution of improvement scores. Because of the robustness of a t-test, it is
appropriate to use a paired t-test for these data.
The Independent Samples t-Test
The independent samples t-test compares the means of two independent groups.
The assumptions of this test are that the two groups are independent of each other, the
dependent variable must be measured on an interval or ratio level, and the scores should
be normally distributed. All assumptions have been met for this test (refer to Figure 4-1)
for distribution of mean improvement scores.
Z Std. Dev = 4.41
Mean = .8
-8.0 -4.0 0.0 4.0 8.0 12.0
-6.0 -2.0 2.0 6.0 10.0
AD Day 1 Minus AD day 4
Figure 4-1. Distribution of mean improvement scores for total sample (N = 39). Mean
and standard deviation of the improvement in SBP estimation for the entire
sample of hypertensive persons is provided.
The mean actual SBP and estimated SBP across all study days was 136.5 and
136.1 mmHg, respectively. The mean difference across all study days was + 0.43
mmHg. This finding suggests that subjects were extremely accurate in estimating their
SBP; however, the mean difference does not take into account the variability of SBP
measurement/estimations and the over- and underestimators of SBP. The absolute value
of the difference between estimated and actual SBP for each subject was calculated and
averaged and was found to be 8.6 mmHg. Therefore, subjects were actually estimating
on average within + 8.6 mmHg of their actual SBP level across all study days. The AD
was calculated and used in this study to take into consideration that there would be over-
and underestimations of SBP and to gain the true picture of SBP elimination. This
method has been used by Luborsky et al. (1976) in a similar BP estimation study.
Hypothesis 1. Adult hypertensives differ significantly in their mean AD after the
ambulatory BP awareness training intervention, compared with before the
For hypothesis 1, the mean absolute difference of day 1 was compared to the
mean absolute difference of day 4, using a paired-samples t-test. The mean absolute
difference on day 1 (pretraining) was 10.1 + 3.5 mmHg and the mean absolute difference
on day 4 (posttraining) was 9.29 3.2 mmHg. The hypertensive subjects improved their
mean scores after the training, however the improvement was not statistically significant
(t = 1.094, df = 38, p = 0.281). Of the 39 subjects, 18 subjects showed no improvement
and 21 subjects (54%) showed improvement in estimating their SBP after the training.
See Figure 4-1 for a graphical display of the AD of day 1 minus the AD of day 4 (mean
improvement) of the total hypertensive sample. As Figure 4-1 shows, the mean
improvement was 0.8 4.4 mmHg for the total sample of hypertensive subjects (N = 39).
Hypothesis 2. College-educated hypertensives differ significantly from noncollege-
educated hypertensives in their mean improvement of SBP estimation.
For hypothesis 2, CE hypertensives were compared to NCE hypertensives to
assess differences in their mean improvement scores for day 1 and day 4. The CE
subgroup was composed of 15 subjects (6 males, 9 females), mean age 43.2 13.7, mean
BMI = 29.02, and mean improvement 2.0 + 4.1 mmHg. The NCE subgroup was
composed of 24 subjects (9 males, 15 females), mean improvement 0.04 4.5 mmHg,
mean age 51.6 years, mean BMI 31.4. The CE and NCE groups had similar marital
status and frequencies of reported tobacco, caffeine, and alcohol use. Compared to CE
subjects, NCE subjects were older (p = 0.05), more frequently taking medications for
hypertension (p = 0.05), and had more family cardiovascular disease history (p = 0.05).
In addition, trends in NCE subjects included a longer personal history of hypertension,
less alcohol use, and had a greater African American racial percentage; however, these
were not statistically significant compared with CE subjects. The mean actual SBP for
the CE group was significantly lower compared to the NCE group on day 1; 132.8 mmHg
and 139.6 mmHg respectively (p = 0.05). Similarly, the mean SBP on day 4 was lower
for the CE group, however not significantly (p = 0.108). Refer to Tables 4-1, 4-2, 4-3,
and 4-5 for demographic, health status, lifestyle factors, and clinical data for these
To test hypothesis 2, an independent samples t-test was used. The difference
between the two groups was not statistically significant (t = -1.333, df= 37, p = 0.19).
The mean improvement scores of NCE hypertensives (mean improvement 0.04 4.5
mmHg) were not significantly different than the mean improvement of CE hypertensives
(mean improvement = 2.0 + 4.1 mmHg). Because the analysis performed in hypothesis 2
is comparing the two independent groups improvement using an independent samples
t-test, it is unclear if the college-educated group alone improved significantly between
day 1 and day 4. Therefore, a paired-samples t-test was performed to assess the change
in mean AD from day 1 to day 4 among the CE subjects.
Hypothesis 3. College-educated hypertensives decrease their mean AD post-training
compared to pretraining.
A paired samples t-test was calculated to compare the pretraining mean AD to the
posttraining mean AD among CE hypertensives. The mean AD on day 1 was 9.74 3.4
mmHg and the mean AD on day 4 was 7.78 2.0 mmHg. A significant decrease in
mean AD from pretraining to posttraining was found using a one-tailed test (t = 1.86, df
=14, p = 0.04). This supports the hypothesis that CE hypertensives improve their
accuracy significantly after training. Refer to Tables 4-1, 4-2, and 4-3 for a description
of the demographic, health status, and lifestyle factors data of the CE subjects. Refer to
Table 4-5 for a description of the clinical characteristics of the group of CE
hypertensives, expressed using means and standard deviations.
An independent samples t-test was calculated to compare the mean improvement
scores of female CE hypertensives compared to mean improvement scores of male CE
hypertensives. The mean improvement scores for female CE hypertensives (N = 9) was
3.31 4.76 mmHg. The mean improvement for male CE hypertensives was -0.093
1.17 mmHg. This difference between groups approached, but did not reach statistical
significance (p = 0.069). As shown in Figure 4-2, male CE hypertensives actually
worsened their ability to estimate their SBP after the training, while the female CE
hypertensives improved at near statistically significant levels (p = 0.069).
Table 4-5. Clinical characteristics of college-educated hypertensives (N = 15).
Actual SBP (mmHg)
Number of ASBP-
*132.8 + 10.3
12.8 + 2.9
(N = 24)
rnin Day 1 Day 4
196.0 + 46.2
132.1 + 11.3
132.7 + 10.6
7.8 + 2.0*
*139.6 + 10.8
138.1 + 9.2
10.3 + 3.7
138.5 + 12.1
138.2 + 12.2
Values are expressed as means standard deviations.
* p < 0.05 versus pretest scores by paired t-test within groups or independent samples t-tests between groups.
.E Today 1
Figure 4-2. Gender effects on estimation of SBP among college-educated hypertensives
Hypothesis 4. Hypertensives with a BMI <30 differ significantly than hypertensives with
a BMI > 30 in their mean improvement.
To test the hypothesis that hypertensives with a BMI < 30 differ significantly than
hypertensives with a BMI > 30 in their mean improvement, an independent samples t-test
was used. The BMI < 30 group was composed of 17 subjects; 3 males and 14 females.
The BMI > 30 group was composed of 22 subjects; 12 males and 10 females. Compared
to BMI < 30 group, subjects with BMI > 30 had significantly more males (p = 0.02),
asthma (p = 0.05) and showed trends toward more chronic pain history (p = 0.06) and
less exercise (p = 0.09). The mean actual SBP for the BMI < 30 group (N= 17) was
greater than the mean actual SBP of the BMI > 30 group of subjects; however this
difference was not statistically significant. The BMI < 30 groups' mean actual SBP was
139.5 on day 1 and 138.2 on day 4. The BMI > 30 group had a mean actual SBP of
135.1 mmHg on day 1 and 134.5 mmHg on day 4.
An independent samples t-test was calculated to compare the mean improvement
score of the BMI < 30 subgroup with the mean improvement score of the BMI > 30
subgroup. The mean improvement score of the BMI < 30 subgroup was .9 + 3.9 mmHg
and the mean improvement score for the BMI > 30 subgroup was .7 4.9 mmHg. The
mean improvement scores of the BMI < 30 group were not statistically different than the
mean improvement scores of the BMI > 30 group (t = -.158, df= 37, p = .875).
Figure 4-3 shows the effects of BMI level on estimation of SBP as measured by absolute
differences of actual and estimated SBP for days 1 and 4. As shown in Figure 4-3, both
subgroups of BMI had decreases in their mean AD between day 1 and day 4; however,
these trends were not statistically significant.
M 10 9.7 9.64
cmr 10 f
BMI less than 30 BMI greater than 30
Figure 4-3. BMI Effects on Estimation of SBP in Total Sample (N = 39).
Hypothesis 5. Male hypertensives differ significantly in their mean improvement,
compared with female hypertensives.
To test the hypothesis that male hypertensives differ significantly in their mean
improvement, compared with female hypertensives, an independent samples t-test was
performed. There were 15 male subjects and 24 female subjects. Comparing both
groups, male mean age was 45.1 years versus 50.4 years (p = 0.17) and mean BMI was
32.3 versus 29.3 (p = 0.06). The groups differed significantly in terms of medication use
(p = 0.02) and medication type (p = 0.01). Among females, 96% reported taking one
medication on a daily basis compared with 67% males. Seventy percent of females
reported taking antihypertension medications, whereas only 40% of males reported
taking hypertension medications. Mean BMI for males was higher than females (32.3
kg/m2 versus 29.3 kg/m2 respectively) (p = 0.07). Actual SBP levels for days 1 and 4
were not significantly different between males compared to females. Interestingly,
female subjects mean actual SBP decreased from 136.6 mmHg on day 1 to 134.8 mmHg
on day 4. The mean actual SBP was also lower for the females compared with the males.
Additionally, the males' mean actual SBP increased between days 1 and 4, while the
females' mean actual SBP decreased. These trends in mean SBP were not found to be
An independent t-test was calculated comparing the mean improvement scores of
male hypertensive subjects to female hypertensive subjects. No significant differences
were found (t = -.752, df = 37, p = .457). The mean improvement of the male
hypertensives (0.1 + 4.4 mmHg) was not significantly different than the mean
improvement of the female hypertensives (1.2 4.5 mmHg). Figure 4-4 shows the
effects of gender on estimation of SBP among the total sample of hypertensive subjects
(N = 39).
Hypothesis 6. Hypertensives < 48 years of age differ significantly compared to
hypertensives > 48 years and older.
To test the hypothesis that hypertensives < 48 years of age differ significantly
compared to hypertensives > 48 years and older, an independent samples t-test was
performed. The < 48 years of age group was composed of 24 subjects (8 males and 16
females). The > 48 years of age group was composed of 15 subjects (7 males and 8
females). Both groups were similar for all demographic variables except education level
(p = 0.03). Sixty percent of younger subjects were college-educated compared with 25%
for the older group. The mean actual SBP for the < 48 years of age group was 130.8
mmHg for day 1 and 131.3 mmHg for day 4. The mean actual SBP for the > 48 years of
age group was 140.9 mmHg for day 1 and 139.0 mmHg for day 4. The < 48 years of age
group had significantly lower actual SBP than the > 48 years of age group on days 1 and
4 (p = 0.004 and p = 0.05 respectively by independent samples t-test).
a 9.5 5
S 9 9
Day 1 Day 4
Figure 4-4. Gender Effect on Estimation of SBP in Total Sample (N = 39).
An independent samples t-test was calculated comparing the mean improvement
of hypertensives less than 48 years of age to hypertensives aged 48 years and older. The
mean improvement of hypertensives less than 48 years of age (0.9 2.9 mmHg) was not
significantly different than the mean improvement of hypertensives 48 years of age and
older (0.71 5.2 mmHg). No significant difference was found (t = .117, df = 37, p =
.907). Refer to Figure 4-5 for graphical presentation of these results.
Age less than 48 Age greater or equal 48
Figure 4-5. Age and Estimation of SBP in Total Sample (N = 39).
Hypothesis 7. Hypertensives using antihypertension medication differ significantly in
their mean improvement compared with hypertensives not taking
To test the hypothesis that hypertensives using antihypertension medication differ
significantly in their mean improvement compared with hypertensives not taking
medications, an independent samples t-test was performed. The HM nonuser and HM
user subjects were similar in age, marital status, and education level. The HM nonuser
subjects trended to be more overweight, had the diagnosis of hypertension longer, and
had higher actual and estimated SBP compared with the HM users; however, these trends
were not significant. The HM users mean SBP on days 1 and 4 were similar to the HM
nonusers; with a mean actual SBP of 136.5 for HM users and 137.7 for HM nonusers for
both days. Refer to Table 4-6 for a description of the HM users and nonusers. Values
are expressed as means + standard deviations, frequencies, and percentages.
An independent samples t-test was calculated comparing the mean improvement
of hypertensives using HM (N = 23) to hypertensives not using medication (N = 16). A
significant difference was found between groups (t = 2.038, df = 37, p = 0.05) for a two-
tailed test (p < 0.05). Figure 4-6 compares the mean improvement between both groups.
The mean improvement of the HM nonuser group (2.4 5.2 mmHg) was significantly
better than the group using HM (-.4 + 3.4 mmHg).
Table 4-6. Description of antihypertension medication user and nonusers
Time with diagnosis
Less than 5 years
21 or more years
ASBP day 1, mmHg
ESBP day 1, mmHg
ASBP day 4, mmHg
ESBP day 4, mmHg
AD day 1, mmHg
AD day 4, mmHg
Mean improvement, mmHg
Number of observations day 1
Number of observations day 4
(N = 23)
49.2 + 10.7
6 males, 17 females
29.6 + 5.5
136.4 + 12.0
135.1 + 14.0
10.1 + 3.1
-.4 + 3.4
12.0 + 1.8
12.5 + 1.7
47.2 + 12.8
9 males, 7 females
137.5 + 10.0
8.1 + 3.0*
12.0 + 1.8
As shown in Figure 4-7, gender has an effect on estimation of SBP among
subjects who are not taking HM (N =16). Female hypertensives that didn't take
medications for hypertension (N = 7) were compared to male hypertensives that didn't
take medications for hypertension (N = 9) using an independent samples t-test. A
significant difference (p = 0.03) was found between the two groups using a two-tailed
test. The mean improvement for hypertensives that did not take HM was 0.06 +
5.4 mmHg for males and 5.5 3.1 mmHg for females. This improvement is also
interesting given the fact that similar findings occurred when comparing CE males and
females. Refer to Table 4-7 for a description of hypotheses and major findings.
HM Non-Users (N = 16) and HM User (N = 23)
Comparison of improvement in SBP estimation between HM nonusers
and HM users. *p< 0.05 by independent sample t-test.
-I 12.88 I
* Day 1
* Day 4
Figure 4-7. Gender effects on estimation of SBP among HM nonusers (N = 16).
Female scores statistically different than male scores at p < 0.05 level by
independent sampled t-test.
HMM r Jon-userS
Table 4-7. Summary of major outcome measures for each hypothesis
H1 TS (N = 39)
CE (N 15)
CE (N 15)
Day 1 mean
with day 4
Day 1 mean
with Day 4
Mean AD D1 10.1
Mean AD D4 9.3
MI 0.8 mmHg
MI CE = 2.0 mmHg
MINCE = 0.04 mmHg
Mean AD D1 9.74
Mean AD D4 7.8
MI 2.0 mmHg
*p = 0.042
H4 BMI < 30 Compare both Independent MI BMI< 30 0.9 mmHg
(N 17) & groups mean samples t-test
BMI> 30 improvement MI BMI> 30 0.7 mmHg
H5 Males (15) & Compare both Independent MI males 0.1 mmHg
females (24) groups mean samples t-test MI females 1.2 mmHg
H6 Age < 48 Compare both Independent MI age < 48 0.9 mmHg
(N 15) & groups mean samples t-test MI age > 48 0.7 mmHg
Age > 48 improvement
H7 HM nonuser Compare both Independent MI HM nonuser 2.43
(N = 16) & groups mean samples t-test mmHg
HM user improvement MI HM user -0.4 mmHg
(N 13) p = 0.05
* Note: TS =total sample, CE = college educated, NCE = noncollege-educated, MI=
mean improvement, HM = hypertension medication, BMI = body mass index.
Analysis of Covariance
It is useful to determine if there are any covarying factors that are significantly
related to mean improvement of estimating SBP. A one-way between subjects
ANCOVA (analysis of covariance) allows the investigator to remove the effect of a
known covariate, thereby providing a method of statistical control. An ANCOVA was
performed to examine the effects of gender and hypertension medication use on the total
sample mean improvement scores, covarying out the effects of BMI and age. The
corrected model was significantly related to mean improvement in estimation of SBP
between days 1 and 4 (p = 0.05). The main effect of hypertension medication use was
significantly related to mean improvement (p = 0.05), with nonusers of hypertension
medication having greater improvement (2.4 + 5.2 mmHg) than users of hypertension
medication (-.4 + 3.4 mmHg). The interaction between hypertension medication use and
gender was also significantly related to mean improvement (p = 0.03). These effects
were seen after taking into account BMI and age. Both BMI (p = 0.5) and age (p = 0.9)
were not significantly related to mean improvement scores.
Reporting Symptoms and Estimating SBP
Among the total hypertensive sample, 14 (36%) participants reported symptoms
associated with high BP. Reported symptoms included tenseness, flushing, and
headache. A greater improvement (1.14 4.9 mmHg) was seen in the 14 subjects who
reported symptoms associated with elevated BP compared to the 25 subjects who did not
report symptoms (0.6 + 3.5 mmHg). An independent samples t-test was performed to
compare the mean improvement scores of subjects who reported experiencing symptoms
with those who did not. No significant differences were found (t = -.38, df= 37, p =
0.71). Refer to Figure 4-8 for a description of this data.
Among hypertensives that do not take HM, 13 subjects reported not experiencing
symptoms relating to their high BP levels and 3 reported experiencing symptoms relating
to their high BP levels. The mean improvement of those subjects is shown in Figure 4-9.
The mean improvement of subjects who did not take HM and reported symptoms
associated with high BP levels (N=3) improved an average of 4.14 mmHg after training.
Subjects who did not report symptoms associated with their SBP and who were not using
HMs (N = 13) improved an average of 2.03 mmHg after training. The small numbers of
participants in each group and the uneven distribution of subjects per group make this
comparison difficult and more inquiry is needed.
o6 6 EDay 4
Figure 4-8. Reporting of symptoms associated with high BP and SBP estimation.
4.5 .4 14
E 3.5 -
2 2.5 u
E 2- yes
Figure 4-9. Reporting of symptoms among nonusers of HM (N = 16).
High BP Estimation
Because of the repeated measures design of the study, absolute differences can be
computed for repeated measures of actual SBP and estimated SBP. A total of 1847 BP
measurements/estimations were analyzed. Using SPSS, a filter variable was created by
selecting only cases that were less than 140 mmHg (N = 1095). The mean AD across all
days was compared between cases that were < 140 mmHg compared with cases that were
S140 mmHg. There were statistically significant differences between the two groups
using an independent samples t-test (t = 4.13, df = 1845, p = 0.001). The mean AD
across all days for the > 140 mmHg group of cases was 9.37 + 7.4 and the mean AD
across all days for the < 140 mmHg group of cases was 8.0 + 6.7 mmHg. The less than
140 mmHg group of cases (N = 1095) had a mean AD on days 1, 2, and 3, and 4 of 9.9
mmHg, 6.6 mmHg, and 8.8 mmHg, respectively. The greater than or equal to 140
mmHg group of cases (N = 752) had a mean AD on days 1, 2, and 3, and 4 of 10.0
mmHg, 8.7 mmHg, and 9.9 mmHg, respectively.
DISCUSSION AND RECOMMENDATIONS
All descriptive and analytic results that addressed each research hypothesis will
be discussed in this chapter. Conclusions and implications for clinical practice as well as
recommendations for future research will also be provided.
Discussion of Results
This study was unique in its design and attempts to directly focus on
hypertensives and provide both physiological and self-awareness feedback, especially
using a repeated measures design and ambulatory BP monitoring. Similar studies have
undertaken the task of determining the effects of feedback on BP estimation (Barr et al.,
1988; Cinciripini et al., 1979; Greenstadt et al., 1988; Luborsky et al., 1976). However,
the present study is the first to examine the effects ofbiosituational feedback using
ambulatory monitoring on the estimation of SBP in adult hypertensive persons. Prior
studies were composed ofnormotensive, younger, male samples. In addition, this study
sought to uncover differences in estimation of SBP among a population of adult
hypertensives and also between different sub-groups of the sample.
For hypothesis 1, hypertensive subjects' day 1 mean absolute difference between
actual and estimated SBP was compared to their day 4 mean absolute difference using a
paired-samples t-test. The mean absolute difference on day 1 was 10.1 mmHg. The
mean absolute difference on day 4 was 9.3 mmHg. These findings indicate that subjects