Blood Pressure Regulation

Blood Pressure Regulation
 Three major components of the circulatory system: blood volume, cardiac pump, and vasculature.
 They must respond effectively to complex neural, chemical, and hormonal feedback systems to
maintain an adequate blood pressure (BP) and perfuse body tissues.
 BP is regulated through a complex interaction of neural, chemical, and hormonal feedback
systems affecting both cardiac output and peripheral resistance.
 This relationship is expressed in the following equation: Mean arterial BP = CO × PR
 Cardiac output is a product of the stroke volume (the amount of blood ejected from the left
ventricle during systole) and heart rate.
 Peripheral resistance is primarily determined by the diameter of the arterioles.
 Tissue perfusion and organ perfusion depend on mean arterial pressure (MAP), or the average
pressure at which blood moves through the vasculature.
 MAP must exceed 65 mm Hg for cells to receive the oxygen and nutrients needed to metabolize
energy in amounts sufficient to sustain life.
 True MAP can be calculated only by complex methods; however, most digital BP machines provide
a MAP reading to guide clinical decisions.
 BP is regulated by baroreceptors (pressure receptors) located in the carotid sinus and aortic arch.
 These pressure receptors are responsible for monitoring the circulatory volume and regulating
neural and endocrine activities.
 When BP drops, catecholamines (epinephrine, norepinephrine) are released from the adrenal
medulla. These increase heart rate and cause vasoconstriction, restoring BP. Chemoreceptors,
also located in the aortic arch and carotid arteries, regulate BP and respiratory rate using much
the same mechanism in response to changes in oxygen and carbon dioxide (CO2 ) concentrations in
the blood. These primary regulatory mechanisms can respond to changes in BP on a moment-to-
moment basis.
 The kidneys regulate BP by releasing renin, an enzyme needed for the eventual conversion of
angiotensin I to angiotensin II, a potent vasoconstrictor. This stimulation of the renin–angiotensin
mechanism and the resulting vasoconstriction indirectly lead to the release of aldosterone from
the adrenal cortex, which promotes the retention of sodium and water (hypernatremia).
Hypernatremia then stimulates the release of antidiuretic hormone (ADH) by the pituitary gland.
ADH causes the kidneys to retain water further in an effort to raise blood volume and BP. These
secondary regulatory mechanisms may take hours or days to respond to changes in BP.
 The relationship between the initiation of shock and the responsiveness of primary and secondary
regulatory mechanisms that compensate for deficits in blood volume, the pumping effectiveness
of the heart, or vascular tone, which may result because of the shock state, is noted in Figure 11-2.
 Beginning with ventricular systole, the pressure inside the ventricles rapidly increases, forcing
the AV valves to close. As a result, blood ceases to flow from the atria into the ventricles, and
regurgitation (backflow) of blood into the atria is prevented.
 The rapid increase in pressure inside the right and left ventricles forces the pulmonic and aortic
valves to open, and blood is ejected into the pulmonary artery and aorta, respectively.
 The exit of blood is at first rapid; then, as the pressure in each ventricle and its corresponding
artery equalizes, the flow of blood gradually decreases.
 At the end of systole, pressure within the right and left ventricles rapidly decreases. As a result,
pulmonary arterial and aortic pressures decrease, causing closure of the semilunar valves.
These events mark the onset of diastole, and the cardiac cycle is repeated.
 Chamber pressures can be measured with the use of special monitoring catheters and
equipment. This technique is called hemodynamic monitoring.
Cardiac Output
Cardiac output refers to the total amount of blood ejected by one of the ventricles in liters per
minute. The cardiac output in a resting adult is 4 to 6 L/min but varies greatly depending on the
metabolic needs of the body. Cardiac output is computed by multiplying the stroke volume by the
heart rate. Stroke volume is the amount of blood ejected from one of the ventricles per heartbeat. The
average resting stroke volume is about 60 to 130 mL
Cardiac Cycle
The cardiac cycle refers to the events that occur in the heart from the beginning of one
heartbeat to the next. The number of cardiac cycles completed in a minute depends on the heart rate.
Each cardiac cycle has three major sequential events: diastole, atrial systole, and ventricular systole.
These events cause blood to flow through the heart due to changes in chamber pressures and
valvular function during diastole and systole.
During diastole, all four heart chambers are relaxed. As a result, the AV valves are open and the
semilunar valves are closed. Pressures in all of the chambers are the lowest during diastole, which
facilitates ventricular filling. Venous blood returns to the right atrium from the superior and
inferior vena cava, then into the right ventricle. On the left side, oxygenated blood returns from the
lungs via the four pulmonary veins into the left atrium and ventricle.
Toward the end of this diastolic period, atrial systole occurs as the atrial muscles contract in
response to an electrical impulse initiated by the SA node. Atrial systole increases the pressure
inside the atria, ejecting the remaining blood into the ventricles. Atrial systole augments ventricular
blood volume by 15% to 25% and is sometimes referred to as the atrial kick. At this point,
ventricular systole begins in response to propagation of the electrical impulse that began in the SA
node some milliseconds earlier.
Effect of Heart Rate on Cardiac Output

The cardiac output responds to changes in the metabolic demands of the tissues associated with
stress, physical exercise, and illness. To compensate for these added demands, the cardiac output is
enhanced by increases in both stroke volume and heart rate. Changes in heart rate are due to
inhibition or stimulation of the SA node mediated by the parasympathetic and sympathetic divisions
of the autonomic nervous system. The balance between these two reflex control systems normally
determines the heart rate. Branches of the parasympathetic nervous system travel to the SA node
by the vagus nerve. Stimulation of the vagus nerve slows the heart rate. The sympathetic nervous
system increases heart rate by innervation of the beta-1 receptor sites located within the SA node.
The heart rate is increased by the sympathetic nervous system through an increased level of
circulating catecholamines (secreted by the adrenal gland) and by excess thyroid hormone, which
produces a catecholamine-like effect. In addition, the heart rate is affected by central nervous system
and baroreceptor activity. Baroreceptors are specialized nerve cells located in the aortic arch and in
both right and left internal carotid arteries (at the point of bifurcation from the common carotid
arteries). The baroreceptors are sensitive to changes in blood pressure (BP). During hypertension
(significant elevations in BP), these cells increase their rate of discharge, transmitting impulses to the
cerebral medulla. This action initiates parasympathetic activity and inhibits sympathetic response,
lowering the heart rate and the BP. The opposite is true during hypotension (low BP). Decreased
baroreceptor stimulation during periods of hypotension prompts a decrease in parasympathetic
activity and enhances sympathetic responses. These compensatory mechanisms attempt to elevate the
BP through vasoconstriction and increased heart rate.
Effect of Stroke Volume on Cardiac Output

Stroke volume is primarily determined by three factors: preload, afterload, and contractility.
Preload refers to the degree of stretch of the ventricular cardiac muscle fibers at the end of diastole.
The end of diastole is the period when filling volume in the ventricles is the highest and the degree of
stretch on the muscle fibers is the greatest. The volume of blood within the ventricle at the end of
diastole determines preload, which directly affects stroke volume. Therefore, preload is commonly
referred to as left ventricular end-diastolic pressure. As the volume of blood returning to the heart
increases, muscle fiber stretch also increases (increased preload), resulting in stronger contraction
and a greater stroke volume. This relationship, referred to as the Frank–Starling (or Starling) law of
the heart, is maintained until the physiologic limit of the muscle is reached. The Frank–Starling law is
based on the fact that, within limits, the greater the initial length or stretch of the sarcomeres
(cardiac muscle cells), the greater the degree of shortening that occurs. This result is caused by
increased interaction between the thick and thin filaments within the cardiac muscle cells. Preload
is decreased by a reduction in the volume of blood returning to the ventricles. Diuresis, venodilating
agents (e.g., nitrates), excessive loss of blood, or dehydration (excessive loss of body fluids from
vomiting, diarrhea, or diaphoresis) reduce preload. Preload is increased by increasing the return of
circulating blood volume to the ventricles. Controlling the loss of blood or body fluids and
replacing fluids (i.e., blood transfusions and intravenous [IV] fluid administration) are examples of ways
to increase preload. Afterload, or resistance to ejection of blood from the ventricle, is the second
determinant of stroke volume. The resistance of the systemic BP to left ventricular ejection is
called systemic vascular resistance. The resistance of the pulmonary BP to right ventricular
ejection is called pulmonary vascular resistance. There is an inverse relationship between afterload
and stroke volume. For example, afterload is increased by arterial vasoconstriction, which leads to
decreased stroke volume. The opposite is true with arterial vasodilation, in which case afterload is
reduced because there is less resistance to ejection, and stroke volume increases. Contractility
refers to the force generated by the contracting myocardium. Contractility is enhanced by circulating
catecholamines, sympathetic neuronal activity, and certain medications (e.g., digoxin, dopamine, or
dobutamine). Increased contractility results in increased stroke volume. Contractility is depressed
by hypoxemia, acidosis, and certain medications (e.g., betaadrenergic–blocking agents such as
metoprolol). The heart can achieve an increase in stroke volume (e.g., during exercise) if preload is
increased (through increased venous return), if contractility is increased (through sympathetic
nervous system discharge), and if afterload is decreased (through peripheral vasodilation with
decreased aortic pressure). The percentage of the end-diastolic blood volume that is ejected with
each heartbeat is called the ejection fraction. The ejection fraction of the normal left ventricle is 55%
to 65%. The right ventricular ejection fraction is rarely measured. The ejection fraction is used as a
measure of myocardial contractility. An ejection fraction of less than 40% indicates that the patient
has decreased left ventricular function and likely requires treatment of HF.

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Blood Pressure Regulation

Effect of Heart Rate on Cardiac Output

Effect of Stroke Volume on Cardiac Output

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