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Hypertension. Por: Marsh, Charles C., Pharm D, Rizzo, Connie, MD, Magills
Medical Guide (Online Edition), January, 2014

Anatomy or system affected:Blood vessels, brain, circulatory system, heart,

kidneys, urinary system
Definition:An abnormally high blood pressure, an often silent cardiovascular
condition that may lead to heart attack, stroke, and major organ failures.
Causes and Symptoms
Hypertension is a higher-than-normal blood pressure (either systolic or
diastolic). Blood pressure is usually measured using a sphygmomanometer and
a stethoscope. The stethoscope is used to hear when the air pressure within
the cuff of the sphygmomanometer is equal to that in the artery. When taking a
blood pressure, the cuff is pumped to inflate an air bladder secured around the
arm; the pressure produced will collapse the blood vessels within. As cuff
pressure decreases, a slight thump is heard as the artery snaps open to allow
blood to flow. At this point, the cuff pressure equals the systolic blood pressure.
As the cuff pressure continues to fall, the sound of blood being pumped will
continue but become progressively softer. At the point where the last sound is
heard, the cuff pressure equals the diastolic blood pressure.
Blood pressure is measured in two numbers: systolic pressure (the pressure of
the blood as it flows out when the heart contracts) over diastolic pressure (the
pressure of the blood within the artery as it flows in when the heart is at rest).
In hypertension, both systolic and diastolic blood pressures are usually
elevated. Blood pressures are reported as the systolic pressure over the
diastolic pressure, such as 130/80 millimeters of mercury. It is important to
recognize there are degrees of seriousness for hypertension. The higher the
blood pressure, the more rigorous the treatment may be. When systolic
pressures are in the high normal range, the individual should be closely
monitored with annual blood pressure checks. Persistently high blood pressures
(greater than 140159/9099 millimeters of mercury) require closer monitoring
and may result in a decision to treat the condition with medication or other
types of intervention.
The blood pressure in an artery is determined by the relationship among three
important controlling factors: the blood volume, the amount of blood pumped
by the heart (cardiac output), and the contraction of smooth muscle within
blood vessels (arterial tone). To illustrate the first point, if blood volume
decreases, the result will be a fall in blood pressure. Conversely, the body
cannot itself increase blood pressure by rapidly adding blood volume; fluid
must be injected into the circulation to do so.

A second controlling factor of blood pressure is cardiac output (the volume of

blood pumped by the heart in a given unit of time, usually reported as liters per
minute). This output is determined by two factors: stroke volume (the volume
of blood pumped with each heartbeat) and the heart rate (beats per minute).
As heart rate increases, output generally increases, and blood pressure may
rise as well. If blood volume is low, such as with excessive bleeding, the blood
returning to the heart per beat is lower and could lead to decreased output. To
compensate, the heart rate increases to prevent a drop in blood pressure.
Therefore, as cardiac output changes, blood pressure does not necessarily
Last, a major controlling factor of blood pressure is arterial tone. Arteries are
largely tubular, smooth muscles that can change their diameter based on the
extent of contraction (tone). This contraction is largely under the control of a
specialized branch of the nervous system called the sympathetic nervous
system. An artery with high arterial tone (contracted) will squeeze the blood
within and increase the pressure inside. There is also a relaxation phase that
will allow expansion and a decrease in blood pressure. Along with relaxation,
arteries are elastic to allow some stretching, which may further help reduce
pressure or, more important, help prevent blood pressure from rising.
There are two general types of hypertension: essential and secondary.
Secondary hypertension is attributable to some underlying identifiable cause,
such as a tumor or kidney disease, while essential hypertension has no
identifiable cause. Therefore, essential hypertension is a defect that results in
excessive arterial pressure secondary to poor regulation by any one of the
three controlling factors discussed above. Each factor can serve as a focal point
for treatment with medications.
The negative consequences of hypertension are mainly manifested in the
deteriorating effect that this condition has on coronary heart disease (CHD).
Cardiovascular risk factors for CHD are described as two types, unmodifiable
and modifiable. Unmodifiable risk factors cannot be changed. This group
includes gender, race, advanced age, and a family history of heart disease
(hypertensive traits can be inherited). The modifiable risk factors are cigarette
smoking (or other forms of tobacco abuse), high blood cholesterol levels,
control over diabetes, and perhaps other factors not yet discovered. For
example, additional factors are now recognized for their adverse effects on
hypertension, including obesity, a lack of physical activity, and psychological
There is no definitive blood pressure level at which a person is no longer at risk
for CHD. While any elevation above the normal range places the person at
increased risk for CHD, what are considered high normal blood pressures were
previously defined as normal. (Looking back at older data, researchers noted
that persons able to maintain pressures at or below 139/89 millimeters of
mercury had less severe CHD.) The definition of normal blood pressure may
change again in the future as new information is discovered. There is a

practical limit as to how low pressure can be while maintaining day-to-day

In coronary heart disease, the blood supply to the heart is reduced, and the
heart cannot function well. The common term for arteriosclerosis, hardening of
the arteries, indicates the symptom of reduced blood flow, which is a major
component of CHD. When the heart cannot supply itself with the necessary
amount of blood (a condition known as ischemia), a characteristic chest pain
called angina may be produced. The hardening aspect of this disease is the
result of cholesterol deposits in the vessel, which decrease elasticity and make
the vessel wall stiff. This stiffness will force pressures in the vessel to increase
if cardiac output rises. As pressures advance, the vessel may develop weak
spots. These areas may rupture or lead to the development of small blood clots
that may clog the vessel; either problem will disrupt blood flow, making the
underlying CHD worse. Eventually, if the blood supply is significantly reduced, a
myocardial infarction(heart attack) may occur. Where the blood supply to the
heart muscle itself is functionally blocked, that part of the heart will die.
Besides contributing to an increased risk of heart attack and coronary heart
disease, hypertension is a major risk for other vascular problems, such as
stroke, kidney failure, heart failure, and visual disturbances secondary to the
effects on the blood vessels within the eye. Hypertension is a major source of
premature death in the United States. According to the Centers for Disease
Control and Prevention in 2014, over 67 million Americans, or 1 in 3 adults,
have hypertension. Over forty percent of all African Americans and over 60
percent of those over the age of sixty-five are affected. Public awareness of
hypertension is increasing, yet less than half of all patients diagnosed are
treated or report having their condition under control. This lack of control is of
particular concern when one considers the organs influenced by hypertension,
most notably the brain, eyes, kidneys, and heart.
Although causative factors of hypertension cannot be identified, many
physiological factors contribute to hypertension. They include increased
sympathetic nervous activity (part of the autonomic nervous system), which
promotes arterial contraction; overproduction of an unidentified sodiumretaining hormone or chronic high sodium intake; inadequate dietary intake of
potassium or calcium; an increased or inappropriate secretion of renin, a
chemical made by the kidney; deficiencies of arterial dilators, such as
prostaglandins; congenital abnormalities (birth defects) of resistance vessels;
diabetes mellitus or resistance to the effects of insulin; obesity; increased
activity of vascular growth factors; and altered cellular ion transport of
electrolytes, such as potassium, sodium, chloride, and bicarbonate.
The kidneys are greatly responsible for blood pressure control. They have a key
role in maintaining both blood volume and blood pressure. When kidney
function declines, secondary to problems such as a decrease in renal blood
flow, the kidney will release renin. High renin levels result in activation of the
renin-angiotensin-aldosterone system. The resulting chemical cascade

produces angiotensin II, a potent arterial constrictor. Another chemical released

is aldosterone, an adrenal hormone which causes the kidney to retain water
and sodium. These two actions add to blood volume and increase arterial tone,
resulting in higher blood pressure. Normally, the renin-angiotensin-aldosterone
system protects kidney function by raising blood pressure when it is low. In
hypertensives, the controlling forces seem to be out of balance, so that the
system does not respond appropriately. The renin-angiotensin-aldosterone
system has a negative effect on bradykinin, a chemical that protects renal
function by producing vasodilating prostaglandins that help maintain adequate
renal blood flow. This protection is especially important in elderly individuals,
who may depend on this system to maintain renal function. The system can be
inhibited by medications such as aspirin or ibuprofen, resulting in a recurrence
of hypertension or less control over the existing disease.
Arteries are largely smooth muscles under the control of the autonomic
nervous system, which is responsible for organ function. Yet there is often no
conscious control of organs; for example, one can tell the lungs to take a
breath, but one cannot tell the heart to beat. The autonomic nervous system
has two branches, sympathetic and parasympathetic, that essentially work
against each other. The sympathetic system exerts much control over blood
pressure. Many chemicals and medicines, such as caffeine, decongestants, and
amphetamines, affect blood pressure by mimicking the effects of increased
sympathetic stimulation of arteries.
Numerous factors associated with blood pressure elevations will affect one or
more of the key determinants of blood pressure; they affect one another as
well. An example will show the extent of their relationship. Sodium and water
retention will increase blood volume returning to the heart. As this return
increases, the heart will increase output (to a point) to prevent heart failure.
This higher cardiac output may also raise blood pressure. If arterial vessels are
constricted, pressures may be even higher. This elevated pressure (resistance)
will force the heart to try to increase output to maintain blood flow to vital
organs. Thus, a vicious cycle is started; hypertension can be perceived as a
merry-go-round ride with no exit.
Treatment and Therapy
Blood pressure reduction has a protective effect against cardiovascular disease.
Generally, as blood pressure decreases, arteries are less contracted and are
able to deliver more blood to the tissues, maintaining their function.
Furthermore, this decreased blood pressure will help reduce the risk of heart
attack in the patient with heart disease. With lower pressures, the heart does
not need to work as hard supplying blood to itself or the rest of the body.
Therefore, the demand for cardiac output to supply blood flow is less. This
reduced workload lowers the incidence of angina.
Treatment of hypertensive patients may involve using one to four different
medications to achieve the goal of blood pressure reduction. There are many
types of medications from which to choose: diuretics, sympatholytic agents

(also known as antiadrenergic drugs), beta-blockers (along with one combinedaction alpha-beta blocker), calcium-channel blockers, peripheral vasodilators,
angiotensin-converting enzyme inhibitors, and the newest class, angiotension
receptor inhibitors. The list of available drugs is extensive; for example, there
are fourteen different thiazide-type diuretics and another six diuretics with
different mechanisms of action.
Patients prone to sodium and water retention are treated with diuretics, agents
that prevent the kidney from reabsorbing sodium and water from the urine.
Diuretics are usually added to other medications to enhance those
medications activity. Research into thiazide-type diuretics has shown that
these agents possess mild calcium-channel blocking activity, aiding their ability
to reduce hypertension.
Beta-blocking agents are used less often than when they were first developed.
They work by decreasing cardiac output through reducing the heart rate.
Although they are highly effective, the heart rate reduction tends to produce
side effects. Most commonly, patients complain of fatigue, sleepiness, and
reduced exercise tolerance (the heart rate cannot increase to adapt to the
increasing demand for blood in tissues and the heart itself). These agents are
still a good choice for hypertensive patients who have suffered a heart attack.
Their benefit is that they reduce the risk of a second heart attack by preventing
the heart from overworking.
Calcium-channel blockers were originally intended to treat angina. These
agents act primarily by decreasing arterial smooth muscle contraction. Relaxed
coronary blood vessels can carry more blood, helping prevent the pain of
angina. When calcium ions enter the smooth muscle, a more sustained
contraction is produced; therefore, blocking this effect will produce relaxation.
Physicians noted that this relaxation also produced lower blood pressures. The
distinct advantage to these agents is that they are well tolerated; however,
some patients may require increasing their fiber intake to prevent some
constipating effects.
Peripheral vasodilators have been a disappointment. Theoretically, they should
be ideal since they work directly to cause arterial dilation. Unfortunately, blood
pressure has many determinants, and patients seem to become immune to
direct vasodilator effects. Peripheral vasodilators are useful, however, when
added to other treatments such as beta-blockers or sympatholytic medications.
The sympatholytic agents are divided into two broad categories. The first group
works within the brain to decrease the effects of nerves that would send signals
to blood vessels to constrict (so-called constrict messages). They do this by
increasing the relax signals coming out of the brain to offset the constrict
messages. The net effect is that blood vessels dilate, reducing blood pressure.
Many of these agents have fallen into disfavor because of adverse effects
similar to those of beta-blockers. The second group of sympatholytics works
directly at the nerve-muscle connection. These agents block the constrict
messages of the nerve that would increase arterial smooth muscle tone.

Overall, these agents are well tolerated. Some patients, especially the elderly,
may be very susceptible to their effect and have problems with low blood
pressure; this issue usually resolves itself shortly after the first dose.
The renin-angiotensin-aldosterone system is a key determinant of blood
pressure. Angiotensin-converting enzyme inhibitors (ACE inhibitors) work by
blocking angiotensin II and aldosterone and by preserving bradykinin. They
have been found quite effective for reducing blood pressure and are usually
well tolerated. Some patients will experience a first-dose effect, while others
may develop a dry cough that can be corrected by dose reductions or
discontinuation of the medication. The angiotension receptor inhibitors work,
instead, by blocking the effects of this substance on the target cells of the
arteries themselves. They are proving to be excellent substitutes for people
who cannot tolerate the related class of ACE inhibitors.
Unfortunately, and contrary to popular belief, no one can reliably tell when his
or her own blood pressure is elevated. Consequently, hypertension is called a
silent killer. It is extremely important to have regular blood pressure
evaluations and, if diagnosed with hypertension, to receive treatment.
From 1950 through 1987, as advances in understanding and treating
hypertension were made, the United States population enjoyed a 40 percent
reduction in coronary heart disease and a more than 65 percent reduction in
stroke deaths. (By comparison, noncardiovascular deaths during the same
period were reduced little more than 20 percent.)
It is evident that blood pressure can be reduced without medications. Research
in the 1980s led to a nonpharmacologic approach in the initial management of
hypertension. This strategy includes weight reduction, alcohol restriction,
regular exercise, dietary sodium restriction, dietary potassium and calcium
supplementation, stopping of tobacco use (in any form), and caffeine
restriction. Often, these methods can produce benefits without medication
being prescribed. Stress is another common contributor to hypertension;
therefore, stress reduction and management is another strategy to reduce
blood pressure. This may be achieved through lifestyle changes, meditation,
relaxation techniques, and exercise. Using this approach, medication is added
to the therapy if blood pressure remains elevated despite good efforts at
nonpharmacologic control.
Other aspects of hypertension and hypertensive patients have been identified
to help guide the clinician to the proper choice of medication. With this
approach, the clinician can focus therapy at the most likely cause of the
hypertension: sodium and water retention, high cardiac output, or high
vascular resistance. This pathophysiological approach led to the abandonment
of the rigid step-care approach described in many texts covering hypertension.
The pathophysiological approach to hypertension management is based on a
series of steps that are taken if inadequate responses are seen.

The best strategy for controlling hypertension is to be informed. Each person

needs to be aware of his or her personal risk for developing hypertension. One
should have regular blood pressure evaluations, avoid eating excessive salt and
sodium, increase exercise, and reduce fats in the diet. Maintaining ideal body
weight may be a key control factor. Studies have shown that patients who have
been successful at losing weight will require less stringent treatment. The
benefits could be a need for fewer medications, reduced doses of medications,
or both.
Cruickshank, J. M. Essential (Primary) Hypertension. New York: McGraw-Hill
Medical, 2013. Print.
Elliott, William J., and Henry R. Black. Hypertension: A Companion to
Braunwald's Heart Disease. Philadelphia: Elsevier Saunders, 2013. Print.
"High Blood Pressure Facts." Centers for Disease Control and Prevention. CDC, 7
July 2014. Web. 21 Aug. 2014.
McGowan, Mary P., and Jo McGowan-Chopra. The Hypertension Sourcebook.
Chicago: Contemporary, 2001. Print.
Messerli, Franz H., ed. Cardiovascular Disease in the Elderly. 3d ed. Boston:
Kluwer, 1993. Print.
Mancia, Giuseppe, and Adel E. Berbari. Special Issues in Hypertension. Milano:
Springer-Verlag, 2012. Print.
Matthes, Jan, and Christian Albus. "Improving Adherence with Medication: A
Selective Literature Review Based on the Example of Hypertension Treatment."
Dtsch. Arztebl Int 111.4 (2014): 4147. Print.
Messerli, Franz H. The Heart and Hypertension. New York: Yorke Medical, 1987.
Piscatella, Joseph, and Barry Franklin. Take a Load Off Your Heart: 109 Things
You Can Do to Prevent or Reverse Heart Disease. New York: Workman, 2003.
Portman, Ronald J., Julie R. Ingelfinger, Joseph T. Flynn. "Pediatric
Hypertension." Clinical Hypertension and Vascular Disease. 3d ed. New York:
Humana, 2013. Print.
Rowan, Robert L. Control High Blood Pressure Without Drugs: A Complete
Hypertension Handbook. Rev. ed. New York: Fireside, 2001. Print.
Seeley, Rod R., Trent D. Stephens, and Philip Tate. Anatomy and Physiology. 7th
ed. New York: McGraw-Hill, 2006. Print.
Tierney, Lawrence M., Stephen J. McPhee, and Maxine A. Papadakis, eds.
Current Medical Diagnosis and Treatment 2007. New York: McGraw-Hill, 2006.

Zanchetti, Alberto. "Challenges of Hypertension and Hypertension Treatment."

Journal of Hypertension. Lippincott Williams & Wilkins, 20 Aug. 2014. Web. 24
Aug. 2014.
Derived from: "Hypertension." Magills Medical Guide, Sixth Edition. Salem
Press. 2010.