Tissues can independently alter their blood flow by changing their
vascular resistance. So that this does
not have a knock-on effect elsewhere, the pressure head provided by the mean
arterial blood pressure (MAP) must be controlled. MAP is determined by the total
peripheral resistance (TPR) and cardiac output (MAP = cardiac output
× TPR), which is itself dependent on the central venous pressure (CVP)
(Chapter 20). CVP is highly dependent on the blood volume. Alterations
of any of these variables may change MAP.
Effect of gravity. When standing, the blood pressure at the ankle
is ∼90 mmHg higher than that at the level of the heart, due to the weight of
the column of blood between the two. Similarly, the pressure in the head is ∼30 mmHg
less than that at the level of the heart. Blood pressure is always measured at
the level of the heart. Gravity does not affect the driving force between arteries and veins because arterial and
venous pressures are affected equally.
Acute regulation of the mean
arterial blood pressure: the baroreceptor reflex
Physiological regulation commonly
involves negative feedback. This requires a sensor that detects
the controlled variable (e.g. MAP), a comparator that compares the
sensor output to a set point, and a feedback pathway driving effectors
that adjust the variable until the difference between the sensor output and
the set point is minimized (Chapter 1). The sensor for MAP is provided by baroreceptors
(stretch receptors) located in the carotid sinus and aortic arch (Fig.
22a). A decrease in MAP reduces arterial wall stretch and decreases baroreceptor
activity, resulting in decreased firing in afferent nerves travelling via the
glossopharyngeal and vagus to the medulla of the brain stem, where the activity
of the autonomic nervous system (ANS) (Chapter 7) is coordinated.
Sympathetic nervous activity consequently increases, causing an
increased heart rate and cardiac contractility (Chapter 20), peripheral
vasoconstriction, and an increase in TPR and venoconstriction, which increases
CVP (Chapter 21). Parasympathetic activity decreases, contributing to
the rise in heart rate (Chapter 19). MAP therefore returns to normal (Fig.
22b). An increase in MAP has the opposite effects.
The baroreceptors are most
sensitive between 80 and 150 mmHg, and their sensitivity is increased by a
large pulse pressure (Chapter 16). They also show adaptation; if
a new pressure is maintained for a few hours, activity slowly returns towards
(but not to) normal. The baroreceptor reflex is important for buffering short-term
changes in MAP, e.g. when muscle blood flow increases rapidly in exercise.
Cutting the baroreceptor nerves has a minor effect on average MAP, but
fluctuations in pressure are much greater.
Posture. Changes in posture provide a good example of
the acute baroreceptor reflex. When standing from a supine position, blood
pools in the veins of the legs, causing a fall in CVP; cardiac output and MAP
therefore fall (postural hypotension; Chapter 20). Baroreceptor firing
is reduced and the baroreceptor reflex is activated. Venoconstriction reduces
blood pooling and helps restore CVP which, coupled with an increase in heart
rate and cardiac contractility, returns cardiac output towards normal;
peripheral vasoconstriction assists the restoration of MAP. The
transient dizziness or blackout (syncope) occasionally experienced when
rising rapidly is due to a fall in cerebral perfusion that occurs before
cardiac output and MAP can be corrected.
Long-term regulation: control of
blood volume (Fig. 22c)
The blood volume is dependent on
total body Na+ and water. These are regulated by the kidneys, and it is
therefore strongly recommended that this chapter is read together with Chapter
35, where the renal mechanisms involved are discussed in detail.
The activation of the baroreceptor
reflex by a reduction in MAP leads to renal arteriolar constriction mediated by
efferent sympathetic nerves. This and the fall in MAP itself cause a reduction
in renal perfusion pressure, which reduces glomerular filtration and so
inhibits excretion of Na+ and water in the urine. Sympathetic stimulation and
reduced arteriolar pressure also activate the renin–angiotensin system (Chapter
35) and thus the production of angiotensin II, a potent vasoconstrictor
that increases TPR. Angiotensin II also stimulates the production of aldosterone
from the adrenal cortex, which promotes renal Na+ reabsorption. The net
effect is Na+ and water retention, and an increase in blood volume (Fig. 22d).
Conversely, a rise in MAP increases Na+ and water excretion.
Changes in blood volume are sensed
directly by cardiopulmonary receptors: veno-atrial receptors are located
around the join between the veins and atria, and atrial receptors in the
atrial wall. These effectively respond to changes in CVP and blood volume.
Stimulation (stretch) suppresses the renin–angiotensin system, sympathetic
activity and secretion of antidiuretic hormone (ADH, vasopressin), but
increases release of atrial natriuretic peptide (ANP) from the atria.
Together, these changes promote renal Na+ and water excretion and reduce blood
volume (Chapters 34 and 35). A fall in blood volume will induce the opposite
effects. The cardiopulmonary receptors normally cause tonic depression –
cutting their efferent nerves increases the heart rate and causes
vasoconstriction in the gut, kidney and skeletal muscle, thus raising MAP.
Cardiovascular shock
and haemorrhage Cardiovascular shock. This is an acute condition with inadequate
blood flow throughout the body, commonly associated with a fall in MAP. It can
result from reduced blood volume (hypovolumic shock), profound
vasodilatation (low-resistance shock) or acute failure of the heart to
pump (cardiogenic shock). The most common cause of hypovolumic shock is haemorrhage;
others include severe burns, vomiting and diarrhoea (e.g. cholera).
Low-resistance shock is due to the pro- found vasodilatation caused by
bacterial infection (septic shock) or powerful allergic reactions (e.g.
to bee stings or peanuts; anaphylactic shock).
Haemorrhage. Some 20% of the blood volume can be lost
without significant problems, as the baroreceptor reflex mobilizes blood from
capacitance vessels and maintains MAP. Volume is restored within 24 h because
arteriolar constriction reduces the capillary pressure and fluid moves from
tissues into the plasma (Chapter 23), urine production is suppressed (see
above) and ADH and angiotensin II stimulate thirst. Greater loss (30–50%) can
be survived, but only with transfusion within ∼1 h (the ‘golden hour’)
(Fig. 22d). After this, irreversible
shock generally develops,
which is irretrievable
even with transfusion. This is because the reduced MAP
and consequent profound peripheral vasoconstriction cause tissue ischaemia and
the build-up of toxins and acidity, which damage the microvasculature and
heart and lead to multiorgan failure.
