Ch16.pdf
(
271 KB
)
Pobierz
16
CHAPTER
Alterations in
Blood Pressure
Aging
Bed Rest
Disorders of Autonomic Nervous System Function
Diagnosis and Treatment
Control of Blood Pressure
Determinants of Blood Pressure
Systolic Blood Pressure
Diastolic Blood Pressure
Pulse Pressure
Mean Arterial Pressure
Mechanisms of Blood Pressure Regulation
Short-Term Regulation
Long-Term Regulation
Hypertension
Essential Hypertension
Mechanisms of Blood Pressure Elevation
Contributing Factors
Manifestations
Diagnosis and Treatment
Systolic Hypertension
Secondary Hypertension
Renal Hypertension
Disorders of Adrenocorticosteroid Hormones
Pheochromocytoma
Coarctation of the Aorta
Malignant Hypertension
Hypertension During Pregnancy
Classification
Diagnosis and Treatment
Hypertension in Children
Diagnosis and Treatment
Hypertension in the Elderly
Diagnosis and Treatment
Orthostatic Hypotension
Classification
Causes
Reduced Blood Volume
Drug-Induced Hypotension
B
lood pressure is probably one of the most variable but
best regulated functions of the body. The purpose of the
control of blood pressure is to keep blood flow constant
to vital organs such as the heart, brain, and kidneys. Without
constant flow to these organs, death ensues within seconds,
minutes, or days. Although a decrease in flow produces an im-
mediate threat to life, the continuous elevation of blood pres-
sure that occurs with hypertension is a contributor to pre-
mature death and disability due to its effect on the heart, blood
vessels, and kidneys.
CONTROL OF BLOOD PRESSURE
The arterial blood pressure reflects the rhythmic ejection of
blood from the left ventricle into the aorta. It rises as the left
ventricle contracts and falls as it relaxes. The contour of the ar-
terial pressure tracing shown in Figure 16-1 is typical of the
pressure changes that occur in the large arteries of the systemic
circulation. There is a rapid rise in the pulse contour during left
ventricular contraction, followed by a slower rise to peak pres-
sure. Approximately 70% of the blood that leaves the left ven-
tricle is ejected during the first one third of systole; this ac-
counts for the rapid rise in the pressure contour. The end of
systole is marked by a brief downward deflection and forma-
tion of the dicrotic notch, which occurs when ventricular pres-
sure falls below that in the aorta. The sudden closure of the
aortic valve is associated with a small rise in pressure due to
continued contraction of the aorta and other large vessels
against the closed valve. As the ventricles relax and blood flows
into the peripheral vessels during diastole, the arterial pressure
falls rapidly at first and then declines slowly as the driving force
decreases.
In healthy adults, the highest pressure, called the
systolic
pressure
, ideally is less than 120 mm Hg, and the lowest pres-
sure, called the
diastolic pressure
, is less than 80 mm Hg. The
274
275
Chapter 16: Alterations in Blood Pressure
Systolic pressure (peak)
KEY CONCEPTS
DETERMINANTS OF BLOOD PRESSURE
120
Mean
arterial
pressure
Dicrotic notch
Pulse
pressure
The arterial blood pressure represents the pressure of
the blood as it moves through the arterial system. It
reaches its peak (systolic pressure) as blood is ejected
from the heart during systole and its lowest level
(diastolic pressure) as the heart relaxes during
diastole.
■
80
Diastolic
pressure
(minimum)
Blood pressure is determined by the cardiac output
(stroke volume
×
heart rate) and the resistance that
the blood encounters as it moves through the peri-
pheral vessels (peripheral vascular resistance).
■
40
The systolic blood pressure is largely determined by
the characteristics of the stroke volume being ejected
from the heart and the ability of the aorta to stretch
and accommodate the stroke volume.
■
0
(mm sec)
■
FIGURE 16-1
■
Intra-arterial pressure tracing made from the
brachial artery. Pulse pressure is the difference between systolic
and diastolic pressures. The darker area represents the mean ar-
terial pressure, which can be calculated by using the formula of
mean arterial pressure
=
diastolic pressure
+
pulse pressure/3.
The diastolic pressure is largely determined by the
energy that is stored in the aorta as its elastic fibers
are stretched during systole and by the resistance to
the runoff of blood from the peripheral blood
vessels.
■
difference between the systolic and diastolic pressure (approx-
imately 40 mm Hg) is the
pulse pressure
. The
mean arterial pres-
sure
(approximately 90 to 100 mm Hg), depicted by the darker
area under the pressure tracing in Figure 16-1, represents the av-
erage pressure in the arterial system during ventricular contrac-
tion and relaxation.
Systolic Blood Pressure
The systolic blood pressure reflects the rhythmic ejection of
blood into the aorta (Fig. 16-2). As blood is ejected into the
aorta, it stretches the vessel wall and produces a rise in aortic
pressure. The extent to which the systolic pressure rises or falls
with each cardiac cycle is determined by the amount of blood
ejected into the aorta with each heart beat (
i.e.
, stroke volume),
the velocity of ejection, and the elastic properties of the aorta.
Systolic pressure increases when there is a rapid ejection of a
large stroke volume or when the stroke volume is ejected into
a rigid aorta. The elastic walls of the aorta normally stretch to
accommodate the varying amounts of blood that are ejected
into the aorta; this prevents the pressure from rising excessively
during systole and maintains the pressure during diastole. In
some elderly persons, the elastic fibers of the aorta lose some
of their elasticity, and the aorta becomes more rigid. When this
occurs, the aorta is less able to stretch and buffer the pressure
that is generated as blood is ejected into the aorta, resulting in
an elevated systolic pressure.
Determinants of Blood Pressure
The systolic and diastolic components of blood pressure are de-
termined by the cardiac output and the peripheral vascular re-
sistance and can be expressed as a product of the two (blood
pressure = cardiac output
peripheral vascular resistance). The
cardiac output is the product of the stroke volume (amount of
blood ejected from the heart with each beat) and the heart rate.
The peripheral vascular resistance reflects changes in the radius
of the arterioles as well as the viscosity or thickness of the
blood. The arterioles often are referred to as the
resistance ves-
sels
because they can selectively constrict or relax to control the
resistance to outflow of blood into the capillaries. The body
maintains its blood pressure by adjusting the cardiac output to
compensate for changes in peripheral vascular resistance, and
it changes the peripheral vascular resistance to compensate for
changes in cardiac output.
In hypertension and disease conditions that affect blood
pressure, changes in blood pressure are influenced by the
stroke volume, the rapidity with which blood is ejected from
the heart, the elastic properties of the aorta and large arteries
and their ability to accept various amounts of blood as it is
ejected from the heart, and the properties of the resistance
blood vessels that control the runoff of blood into the smaller
vessels and capillaries that connect the arterial and venous
circulations.
×
Diastolic Blood Pressure
The diastolic blood pressure is maintained by the energy that
has been stored in the elastic walls of the aorta during systole
(see Fig. 16-2). The level at which the diastolic pressure is
maintained depends on the elastic properties of the aorta and
large arteries and their ability to stretch and store energy, the
resistance of the arterioles that control the outflow of blood
into the microcirculation, and the competency of the aortic
valve. The small diameter of the arterioles contributes to their
effectiveness as resistance vessels because it takes more force to
push blood through a smaller vessel than a larger vessel. When
276
Unit Four: Alterations in the Cardiovascular System
peripheral vascular resistance, which maintains the diastolic
pressure.
Systole
Peripheral
resistance
240
250
220
Mean Arterial Pressure
The mean arterial blood pressure represents the average blood
pressure in the systemic circulation. The mean arterial pressure
can be estimated by adding one third of the pulse pressure to
the diastolic pressure (
i.e.
, diastolic blood pressure
230
200
210
180
170
160
150
140
130
pulse
pressure/3). Hemodynamic monitoring equipment in inten-
sive and coronary care units measures or computes mean arte-
rial pressure automatically. Because it is a good indicator of tis-
sue perfusion, the mean arterial pressure often is monitored,
along with systolic and diastolic blood pressures, in critically
ill patients.
+
120
110
100
90
80
70
60
50
40
30
20
10
A
Mechanisms of Blood Pressure Regulation
Although different tissues in the body are able to regulate their
own blood flow, it is necessary for the arterial pressure to re-
main relatively constant as blood shifts from one area of the
body to another. The method by which the arterial pressure is
regulated depends on whether short-term or long-term adap-
tation is needed. The mechanisms of blood pressure regulation
are illustrated in Figure 16-3.
Diastole
240
250
220
230
200
210
180
170
160
150
140
130
120
110
100
90
80
Short-Term Regulation
The mechanisms for short-term regulation of blood pressure,
those occurring over minutes or hours, are intended to cor-
rect temporary imbalances in blood pressure, such as occur
during physical exercise and changes in body position. These
mechanisms also are responsible for maintenance of blood
pressure at survival levels during life-threatening situations.
The short-term regulation of blood pressure relies mainly on
neural and hormonal mechanisms, the most rapid of which are
the neural mechanisms.
70
60
50
40
30
20
10
B
■
FIGURE 16-2
■
Diagram of the left side of the heart. (
A
) Systolic
blood pressure represents the ejection of blood into the aorta dur-
ing ventricular systole; it reflects the stroke volume, the distensi-
bility of the aorta, and the velocity with which blood is ejected
from the heart. (
B
) Diastolic blood pressure represents the pres-
sure in the arterial system during diastole; it is largely determined
by the peripheral vascular resistance.
Neural Mechanisms.
The neural control center for the regu-
lation of blood pressure is located in the reticular formation
of the lower pons and medulla of the brain where integration
and modulation of autonomic nervous system (ANS) responses
occur.
1
This area of the brain contains the vasomotor and car-
diac control centers and is often collectively referred to as the
cardiovascular center. The cardiovascular center transmits para-
sympathetic impulses to the heart through the vagus nerve
and transmits sympathetic impulses to the heart and blood
vessels through the spinal cord and peripheral sympathetic
nerves. Vagal stimulation of the heart produces a slowing of
heart rate, whereas sympathetic stimulation produces an in-
crease in heart rate and cardiac contractility. Blood vessels are
selectively innervated by the sympathetic nervous system. In-
creased sympathetic activity produces constriction of the small
arteries and arterioles with a resultant increase in peripheral
vascular resistance.
The ANS control of blood pressure is mediated through in-
trinsic circulatory reflexes, extrinsic reflexes, and higher neural
control centers. The
intrinsic reflexes
, including the
baroreflex
and
chemoreceptor-mediated reflex
, are located in the circulatory sys-
tem and are essential for rapid and short-term regulation of
blood pressure. The sensors for extrinsic reflexes are found out-
side the circulation. They include blood pressure responses
associated with factors such as pain and cold. The neural path-
there is an increase in peripheral vascular resistance, as with
sympathetic stimulation, diastolic blood pressure rises. Clo-
sure of the aortic valve at the onset of diastole is essential to
the maintenance of the diastolic pressure. When there is in-
complete closure of the aortic valve, as in aortic regurgitation
(see Chapter 17), the diastolic pressure drops as blood flows
backward into the left ventricle, rather than moving forward
into the arterial system.
Pulse Pressure
The pulse pressure is the difference between the systolic and di-
astolic pressures. It reflects the pulsatile nature of arterial blood
flow and is an important component of blood pressure. During
the rapid ejection period of ventricular systole, the volume of
blood that is ejected into the aorta exceeds the amount that
exits the arterial system. The pulse pressure reflects this differ-
ence. The pulse pressure rises when additional amounts of
blood are ejected into the arterial circulation, and it falls when
the resistance to outflow is decreased. In hypovolemic shock,
the pulse pressure declines because of a decrease in stroke vol-
ume and systolic pressure. This occurs despite an increase in
277
Chapter 16: Alterations in Blood Pressure
■
FIGURE 16-3
■
Mechanisms of blood pressure regulation. The
solid lines
represent the mechanisms for
renal and baroreceptor control of blood pressure through changes in cardiac output and peripheral vascu-
lar resistance. The
dashed lines
represent the stimulus for regulation of blood pressure by the baroreceptors
and the kidneys.
ways for these reactions are more diffuse, and their responses
are less consistent than those of the intrinsic reflexes. Many of
these responses are channeled through the hypothalamus,
which plays an essential role in the control of sympathetic ner-
vous system responses. Among higher-center responses are
those due to changes in mood and emotion.
The
baroreceptors
are pressure-sensitive receptors located in
the walls of blood vessels and the heart. The carotid and aortic
baroreceptors are located in strategic positions between the
heart and the brain (Fig. 16-4). They respond to changes in the
stretch of the vessel wall by sending impulses to cardiovascular
centers in the brain stem to effect appropriate changes in heart
rate and vascular smooth muscle tone. For example, the fall in
blood pressure that occurs on moving from the lying to the
standing position produces a decrease in the stretch of the
baroreceptors with a resultant increase in heart rate and sym-
pathetically induced vasoconstriction that causes an increase in
peripheral vascular resistance.
The
arterial chemoreceptors
are sensitive to changes in the oxy-
gen, carbon dioxide, and hydrogen ion content of the blood.
They are located in the carotid bodies, which lie in the bifurca-
tion of the two common carotids, and in the aortic bodies of
the aorta (see Fig.16-4). Because of their location, these chemo-
receptors are always in close contact with the arterial blood.
Although the main function of the chemoreceptors is to regu-
late ventilation, they also communicate with the cardiovascu-
lar center and can induce widespread vasoconstriction. When
the arterial pressure drops below a critical level, the chemo-
receptors are stimulated because of diminished oxygen supply
and a buildup of carbon dioxide and hydrogen ions. In persons
with chronic lung disease, systemic and pulmonary hyperten-
sion may develop because of hypoxemia (see Chapter 21).
Humoral Mechanisms.
A number of hormones and humoral
mechanisms contribute to blood pressure regulation, including
the renin-angiotensin-aldosterone mechanism and vasopressin.
Other humoral substances such as epinephrine, a sympathetic
neurotransmitter released from the adrenal gland, has the effect
of directly stimulating an increase in heart rate, cardiac contrac-
tility, and vascular tone.
The
renin-angiotensin-aldosterone
system plays a central role
in blood pressure regulation. Renin is an enzyme that is syn-
thesized, stored, and released by the kidneys in response to an
increase in sympathetic nervous system activity or a decrease
278
Unit Four: Alterations in the Cardiovascular System
Glossopharyngeal nerve
Extracellular fluid
Arterial blood pressure
Vagus
nerve
Kidney
Carotid
body
Juxtaglomerular cells
Carotid
sinus
Common
carotid
artery
Renin
Angiotensinogen
Angiotensin I
Brachiocephalic
artery
Aortic arch
Lungs
Converting
enzyme
■
FIGURE 16-4
■
Location and innervation of the aortic arch and
carotid sinus baroreceptors and the carotid body chemoreceptors.
Angiotensin II
in blood pressure, extracellular fluid volume, or extracellular
sodium concentration. Most of the renin that is released leaves
the kidney and enters the bloodstream, where it acts enzymat-
ically to convert an inactive circulating plasma protein called
angiotensinogen
to angiotensin I (Fig. 16-5). Angiotensin I trav-
els to the small blood vessels of the lung, where it is converted
to angiotensin II by the angiotensin-converting enzyme that is
present in the endothelium of the lung vessels. Although an-
giotensin II has a half-life of several minutes, renin persists in
the circulation for 30 minutes to 1 hour and continues to cause
production of angiotensin II during this time.
Angiotensin II functions in both the short-term and long-
term regulation of blood pressure. It is a strong vasoconstrictor,
particularly of arterioles and to a lesser extent of veins. The vaso-
constrictor response produces an increase in peripheral vascu-
lar resistance (and blood pressure) and functions in the short-
term regulation of blood pressure. A second major function of
angiotensin II, stimulation of aldosterone secretion from the
adrenal gland, contributes to the long-term regulation of blood
pressure by increasing salt and water retention by the kidney.
It also acts directly on the kidney to decrease the elimination of
salt and water.
Vasopressin,
also known as antidiuretic hormone (ADH), is
released from the posterior pituitary gland in response to de-
creases in blood volume and blood pressure, an increase in the
osmolality of body fluids, and other stimuli. The antidiuretic
actions of vasopressin are discussed in Chapter 6. Vasopressin
has a direct vasoconstrictor effect on blood vessels, particularly
those of the splanchnic circulation that supplies the abdomi-
Adrenal
Cortex
Vasoconstriction
systemic arterioles
Aldosterone
Sodium
reabsorption
by kidney
Arterial blood pressure
Vascular volume and
Arterial blood pressure
■
FIGURE 16-5
■
Control of blood pressure by the renin-
angiotensin-aldosterone system. Renin enzymatically converts the
plasma protein angiotensinogen to angiotensin I; angiotensin-
converting enzyme in the lung converts angiotensin I to angioten-
sin II; and angiotensin II produces vasoconstriction and increases
salt and water retention through direct action on the kidney and
through increased aldosterone secretion by the adrenal cortex.
Plik z chomika:
bibiariel
Inne pliki z tego folderu:
Ch01.pdf
(1284 KB)
Ch02.pdf
(222 KB)
Ch03.pdf
(264 KB)
Ch04.pdf
(253 KB)
Ch06.pdf
(482 KB)
Inne foldery tego chomika:
SecretsSeries_Endocrinology4ed2005McDermott
Zgłoś jeśli
naruszono regulamin