Control of blood pressure and 25 blood volume
-
Upload
others
-
View
2
-
Download
0
Embed Size (px)
Citation preview
PowerPoint PresentationPart 3 The cardiovascular system
54
Physiology at a Glance, Fourth Edition. Edited by Jeremy P.T. Ward
and Roger W.A. Linden. © 2017 John Wiley & Sons, Ltd. Published
2017 by John Wiley & Sons, Ltd. Companion website:
www.ataglanceseries.com/physiology
Control of blood pressure and blood volume25
Figure 25.1 Baroreceptors
Glossopharyngeal
Figure 25.3 Longer term control of blood pressure and volumeFigure
25.2 Acute control of blood pressure
Effectors
Baroreceptors
Starling's law
CO CVPTPR Na+ and water reabsorption Thirst
Figure 25.4 Effect of severe (45%) blood loss: Reversible and
irreversible cardiovascular shock
% in
Transfusion
300 60 90 120
No transfusion: after an initial small recovery in CO due to
activation of baroreceptor reex and uid transfer from tissues,
shock progresses as a result of cardiac and multiorgan
failure
Transfusion at 50min: full recovery
Transfusion at 70min: initially CO recovers, but then declines
irreversibly due to toxins, tissue damage and multiorgan
failure
Example of progression of shock after 45% blood loss:
H ae
m or
rh ag
c25 55 7 February 2017 7:16 PM
55Tissues 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 deter-
mined by the total peripheral resistance (TPR) and cardiac output
(MAP = cardiac output × TPR), which is itself depen- dent on the
central venous pressure (CVP) (Chapter 23). 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 pro- vided by baroreceptors (stretch receptors)
located in the carotid sinus and aortic arch (Figure 25.1). A
decrease in MAP reduces arterial wall stretch and decreases
baroreceptor activity, result- ing in decreased firing in afferent
nerves travelling via the glos- sopharyngeal and vagus to the
medulla of the brain stem, where the activity of the autonomic
nervous system (ANS) (Chap- ter 8) is coordinated. Sympathetic
nervous activity consequently increases, causing an increased heart
rate and cardiac contrac- tility (Chapter 23), peripheral
vasoconstriction and an increase in TPR, and venoconstriction,
which increases CVP (Chapter 24). Parasympathetic activity
decreases, contributing to the rise in heart rate (Chapter 22). MAP
therefore returns to normal (Figure 25.2). 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
19). 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 23).
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 (Figure 25.3) 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 38, 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 38) 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 (Figure 25.4). 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 37 and 38). 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 profound
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 26),
urine production is suppressed (see previously) and ADH and
angiotensin II stimulate thirst. Greater loss (30–50%) can be
survived, but only with transfusion within ∼1 h (the ‘golden hour’)
(Figure 25.4). 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.
Control of blood pressure and blood volume