Biology 221
Anatomy & Physiology II
TOPIC 4
Circulatory System –
Blood Flow, Blood Pressure &
Capillary Dynamics
Chapter 20
pp. 727-747
E. Lathrop-Davis / E. Gorski / S. Kabrhel
1
Blood Flow
• Blood flow is defined as the “volume of blood flowing
through a vessel, an organ, or the entire circulation in a
given period” (Marieb, 2001)
• Flow is measured in ml/min.
• To the entire circulatory system:
– blood flow (BF) is the same as cardiac output (CO);
and
– flow is relatively constant at rest.
• To a specific organ or tissue, flow varies with
demand. Flow increases as tissue activity increases.
2
Blood Flow: Controlling factors
BF = P / R
• Blood flow (BF) equals the change in pressure (P)
between two points divided by the resistance (R) to
flow.
• That is, blood flow is:
– directly proportional to blood pressure gradient
(P) between two points; and
– inversely proportional to peripheral resistance (R)
• Both pressure and resistance are important in
controlling gross body flow.
• Resistance is more important than pressure gradients
in controlling local flow.
3
Resistance to Blood Flow
• Resistance is “a measure of the amount of friction
blood encounters as it passes through vessels”.
• Peripheral resistance (PR) is resistance within the
peripheral vessels (mainly small arteries and
arterioles); it accounts for most resistance in system.
• Resistance is inversely proportional to flow.
Think About It: If something is directly related to
resistance, what affect will it have on blood flow? What
about things that are inversely related to resistance?
4
Resistance to Blood Flow
• Sources of resistance include blood viscosity, total
blood vessel length, and blood vessel diameter.
• Blood viscosity refers to the “thickness” of blood.
– Viscosity is directly proportional to resistance.
– The number of blood cells, especially red blood
cells, affects viscosity directly. More cells means
“thicker” blood.
– Blood volume is relatively minor in terms of
resistance due to its affect on (volume plays an
important role in blood pressure, however):
° Severe dehydration leads to increased viscosity.
° Over-hydration leads to decreased viscosity.
Return to Blood Pressure: Blood Volume
5
Resistance to Blood Flow
• Blood vessel diameter is the main source of resistance.
– Diameter is inversely proportional to resistance.
– Resistance varies as inverse of the radius to the 4th
power (1/r4); i.e., if the radius doubles, resistance
decreases to 1/16 of the original resistance.
– Resistance affecting the whole system is controlled
overall by sympathetic vasomotor tone.
– Resistance affecting tissues is controlled at small
arterioles in response to neural and chemical
controls.
– Any sudden decrease in the size of the lumen (e.g.,
partial blockage) creates turbulence, and thus
increases resistance.
6
Resistance to Blood Flow
• Total blood vessel length refers all the blood vessels in
the body.
– Vessel length is directly proportional to resistance.
– Adipose and tumors lead to angiogenesis, which is
the formation of new blood vessels. Gaining weight
leads an increase in adipose tissue, thus stimulating
angiogenesis and increasing resistance.
Think About It: Which of these 4 factors (viscosity,
volume, vessel diameter, vessel length) would be most
readily controlled?
Return to Blood Pressure: Resistance
7
Blood Pressure (BP)
• Blood pressure is defined as the “force per unit area
exerted on the wall of a blood vessel by its contained
blood”.
• In common usage, “blood pressure” usually refers to
blood pressure in systemic arteries near heart.
• Blood pressure is measured in mm Hg (millimeters of
mercury).
8
Blood Pressure (con’t)
• Blood pressure varies through the vascular system.
• This pressure gradient keeps the blood flowing from
the heart through the arteries, capillaries and back
through the veins.
• Pressure is highest and most variable in aorta and other
elastic arteries.
Think About It: Why would pressure be highest here?
• Pressure decreases through the arterioles and capillaries
so that it is much lower in the veins.
• Pressure is lowest in venae cavae closest to the heart.
Fig. 20.5, p. 729
9
Arterial Blood Pressure
Pressure varies with:
• Age - Older people generally have higher pressure due
to loss of elasticity in the vessel walls.
• Gender - Men generally have higher pressure.
• Weight - Gaining weight leads to angiogenesis, thus
increasing total vessel length (see Resistance).
• Stress level - Stress activates the sympathetic division
of the ANS.
• Mood - Calm thoughts lower pressure; anxiety raises
pressure.
Think About It: By what mechanism do anxiety and
stress affect pressure?
10
Arterial Blood Pressure
Pressure varies with:
• Posture - Pressure is lowest when lying down and
highest when standing.
Think About It: Why would pressure be higher on
standing, lower when lying?
• Physical activity - Pressure is lower at rest and
increases with increased activity.
Think About It: Why would pressure need to increase
during activity.
11
Arterial Blood Pressure
• Arterial blood pressure depends on:
– the compliance (distensibility) of the elastic arteries;
and
– stroke volume (the amount ejected by the heart; See
Topic 2: Heart).
Think About It: How and why does compliance affect
pressure? What would you expect the relationship
between stroke volume and pressure to be?
• Pressure rises as blood is pumped into the arteries
during ventricular systole, and decreases during
diastole when the ventricles relax.
12
Systolic Pressures
Systolic pressure (Ps) is the pressure in arteries during
ventricular systole.
• In a healthy adult, systolic pressure is normally around
110 to 120 mm Hg. Women generally have lower
pressure.
• Systolic pressure occurs when the semilunar valves
open and blood is ejected.
• Compliance of elastic arteries decreases pressure
needed to eject blood into arteries by allowing the
vessels to stretch as blood is added.
• Increased stroke volume (amount ejected) leads to
increased pressure because greater volume is added to
13
the area.
Diastolic Pressures
Diastolic pressure (PD) is the pressure in the arteries
during ventricular diastole.
• In a healthy adult, diastolic pressure is normally
around ~ 70-80 mm Hg.
• Diastolic pressure occurs when the semilunar valves
are closed because the heart is in diastole.
• Elastic recoil of the elastic arteries contributes to
continued pressure and forward movement of blood.
14
Pulse Pressure (PP)
• Pulse pressure is the difference between systolic (PS)
and diastolic (PD) pressures: PP = PS – PD
• Pulse pressure is increased by increased stroke volume
(SV) during exertion, which raises systolic pressure.
• Pulse pressure is also increased by arteriosclerosis, a
degenerative arterial disease characterized by loss of
elasticity, such that it requires much more pressure to
force blood into the vessels during systole.
15
Mean Arterial Pressure (MAP)
• MAP is the average pressure in the main arteries.
• Because the heart spends more time in diastole, MAP
is calculated as diastolic pressure (PD) plus (the pulse
pressure [PP] divided by 3):
MAP = PD + (PP /3)
16
Measuring Pulse
• Pulse is the number of beats per minute. Fig. 20.11, p. 737
• Pulse is measured by palpation of pulse points
(“pressure points”) over the major arteries.
• To measure pulse, one counts the number of
pulsations felt in a given time period.
– Because pulse varies slightly even at rest, the most
accurate count is taken over 60 seconds.
– During heavy exercise, the rate becomes more
variable and it becomes more convenient to count
a shorter time period (e.g., 6 seconds) and
multiply.
• Pulse decreases in strength away from heart.
Think About It: Where would you expect pulse to be strongest? 17
Measuring Arterial Blood Pressure
• Normally, blood pressure is around 120/80 (systolic
pressure of 120 mm Hg; diastolic pressure of 80 mm
Hg) for a healthy, young male
– varies with age, sex, physical condition, gender,
weight, stress, mood, posture
• The auscultatory method is based on the sounds
produced by a partially blocked artery.
– A sphygmomanometer, or blood pressure cuff, is
used with a stethoscope.
18
Measuring Arterial Blood Pressure
• The brachial artery is usually chosen and partially
blocked by inflating the cuff with air to a pressure
greater than normal (usually around 140-150 mm Hg;
higher if hypertension is known or suspected).
• One then listens for Korotkoff sounds, the sounds heard
as blood moves through partially blocked artery.
– The first sound corresponds to the systolic pressure
and occurs as blood first spurts through the vessel.
– The second “sound” is actually when sound is no
longer heard because the pressure in the cuff is
released and blood no longer spurts through the
artery. This occurs during diastole.
19
Capillary Blood Pressures
• “Capillary blood pressure” is the pressure exerted by
blood on capillary walls.
• Within a capillary bed, pressure drops from around 3540 mm Hg at arterial end to around 17-20 mm Hg at
venous end.
• Lower pressure helps prevent breakage of capillary
walls & decreases fluid loss to tissues
Fig. 20.5, p. 729
20
Venous Blood Pressures
• The pressure of blood in the veins is generally low and
steady.
• Venous return is supported by:
– valves in the veins, which prevent backflow of
blood (i.e., maintain unidirectional flow).
° Varicose veins (see Topic 3: Blood Vessels) occur
when valves fail.
21
Venous Blood Pressures
• Venous return is supported by:
– the respiratory pump created by changes in thoracic
and abdominal pressures during breathing.
° During inspiration, thoracic pressure decreases
and abdominal pressure increases, thus blood is
pushed from the abdominal vessels (mainly the
inferior vena cava inferior to the diaphragm) into
the thoracic part of the inferior vena cava. Valves
maintain unidirectional flow during expiration.
22
Venous Blood Pressures (con’t)
• Venous return is supported by:
– the muscular pump in which “milking” by skeleltal
muscle promotes return.
° When skeletal muscle contracts, it puts pressure
on the blood in the vessels; valves prevent the
blood from moving backward; that is, they keep it
moving toward the heart.
° Prolonged inactivity or prolonged contraction
causes blood to pool in the veins, contributes to
varicosities and may allow clots to form. Current
practice is to promote blood movement by leg
massage for bed-ridden patients.
23
Maintaining Blood Pressure
• Blood pressure (BP) varies directly with cardiac
output, and peripheral resistance (blood vessel
diamter), and blood volume.
– That is, increases in any of these lead to increases
in blood pressure.
Fig. 20.7, 20.8
24
Blood Pressure: Cardiac Output
• Review Topic 2 for factors that affect CO.
• CO is controlled by cardiac centers within the reticular
formation of the medulla oblongata (see A&P I: Unit 6 the Brain).
– The cardioacceleratory center (CAC) produces
sympathetic outflow.
° Think About It: What affect will this have on CO?
– The cardioinhibitory center (CIC) produces
parasympathetic outflow.
° Think About It: What affect will this have on CO?
Think About It: What is the relationship between HR and
BP?
Fig. 20.7, 20.8
25
Blood Pressure: Resistance
• Peripheral resistance (PR) is the same as resistance to
blood flow in the peripheral vessels.
– Resistance is directly related to pressure.
° Pressure is needed to overcome resistance; the
greater the resistance, the higher the pressure
needed.
– Blood vessel diameter is the main contributor to
resistance. It is also the most readily controlled.
(Review Sources of Resistance on previous slides.)
Think About It: What relationship would you expect
between blood vessel diameter and BP?
Fig. 20.7, 20.8
26
Blood Pressure: Blood Volume
• Blood volume (BV) is the amount of blood in the
circulatory system.
– BV plays a minor role in peripheral resistance.
– BP varies directly with BV.
– Loss of blood volume due to hemorrhage or severe
dehydration leads to decreased pressure.
– Retention of water leads to increased pressure.
Think About It: What is the relationship between BV
and CO (Review Topic 2)?
Fig. 20.7, 20.8
27
Short-Term Control of Resistance*
• Short-term control of resistance is mainly
accomplished by controlling blood vessel diameter.
• Mechanisms of controlling include neural and
chemical controls
• Goals of controlling BP include:
– altering distribution to meet demands of various
organs/tissues (through controlling vessels); and
– maintaining overall MAP through vasomotor tone
and cardiac output.
Fig. 20.8, p. 733
*Change “resistance” to “blood pressure” on page 48, Section III.B. title.
28
Neural Control of Resistance
The vasomotor center (VMC) controls vasomotor tone
(see Topic 3: Blood Vessels).
• The VMC is located in medulla oblongata (as part of
cardiovascular center).
• It maintains vasomotor tone in all vessels
• Vasomotor fibers are part of the sympathetic division
of the ANS (for the most part, fibers to the vessels of
the external genitalia are part of sacral nerves; see
A&P I: Unit 9 - Autonomic Nervous System).
29
Neural Control of Resistance
• Most vasomotor fibers use norepinephrine (NE) as
their neurotransmitter.
– In these increased sympathetic activity leads to
increased release of NE, which causes
vasoconstriction leading to increased BP.
• Vasomotor fibers to vessels serving skeletal muscle use
acetyl choline (ACh).
– In these increased sympathetic activity leads to
increased release of ACh, which causes vasodilation
leading to increased flow to skeletal muscle
(generally little importance to overall BP).
A&P I Review: Would these be using nicotinic or
30
muscarinic receptors?
Factors Affecting Vasomotor Tone
• Reflexes initiated by baroreceptors or chemoreceptors
are integrated in the cardiovascular centers within the
medulla oblongata (reticular formation; See A&P I:
Unit 6 - Brain)
– The cardiac centers control heart rate and include the
cardiac inhibitory center (CIC) and cardiac
acceleratory center (CAC).
– The vasomotor center controls vasomotor tone
(blood vessel diameter).
31
Baroreceptor-initiated Reflexes
• Baroreceptors (pressoreceptors) are present in the
carotid sinus*, aortic arch*, most other elastic arteries
of neck and thorax. (*main ones)
• Increased BP stimulates baroreceptors.
– Stimulation of the baroreceptors leads to an increase
in afferent impulses to the vasomotor center (VMC).
° These afferent impulses inhibit the VMC,
resulting in decreased sympathetic outflow
leading to relaxation of the smooth muscle of the
vessel walls and vasodilation.
32
Baroreceptor-initiated Reflexes
• Afferent impulses from baroreceptors also go to the
CIC (cardioinhibitory center) in the medulla oblongata
causing an increase parasympathetic outflow to heart.
The afferent impulses also go to the CAC (cardioacceleratory center), which they inhibit, thus decreasing
sympathetic outflow.
• Prolonged hypertension causes baroreceptors to “reset”
to higher pressure.
• Decreases in blood pressure lead to decreases in
afferent impulses sent to the VMC and cardiac centers.
This leads to increases in sympathetic outflow, which
lead to increases in pressure.
33
Chemoreceptor-initiated Reflexes
• Chemoreceptors respond to changes in blood
chemistry.
• Chemoreceptors are located in the aortic arch and the
large arteries of neck, including the carotid arteries.
• Chemoreceptors are connected to the CAC and
vasomotor center (VMC) by afferent fibers.
34
Chemoreceptor-initiated Reflexes
• Chemoreceptors respond to changes in oxygen (O2),
pH (hydrogen ion), or carbon dioxide (CO2) levels.
– Decreases in arterial O2 or pH, or increased CO2
lead to increased impulses to the CAC and
vasomotor center. Stimulation of these centers leads
to increased sympathetic outflow.
° The resulting increased heart rate and
vasoconstriction cause increased BP, which helps
move blood through the system faster and gets
blood to lungs for gas exchange faster.
– CO2 and pH are related in that CO2 combines with
H2O to form carbonic acid (H2CO3).
35
Influence of Higher Brain Centers
on Vasomotor Tone
• The cerebral cortex and hypothalamus are connected to
the cardiovascular center (cardiac centers [CAC and
CIC] and vasomotor center) in the medulla oblongata.
• The hypothalamus:
– responds to threats by mediating the “fight-or-flight”
response. This leads to increased sympathetic
outflow from the CAC and vasomotor center.
– directs changes in flow during activity to increase
flow to skeletal muscle and to control body
temperature.
36
Influence of Higher Brain Centers
on Vasomotor Tone
• Cerebral cortex participates indirectly by influencing
mood and stress responses. In bio-feedback a person
learns to relax, thus increasing parasympathetic
outflow and decreasing sympathetic, resulting in
decreased blood pressure.
37
Short-Term Chemical Control of BP
• Short-term chemical control involves chemicals that
act on vessels or the heart; some also act on blood
volume, thus exerting long-term control.
• These chemicals include:
– Norepinephrine (NE),
– Epinephrine (epi),
– Antidiuretic hormone (ADH),
– Angiotension II,
– Atrial natriuretic peptide (ANP),
– Alcohol (ethanol),
– Inflammatory chemicals, and
– Endothelium-derived factors.
38
Short-Term Chemical Control of BP
• Norepinephrine (NE) released from the adrenal
medulla causes vasoconstriction, especially of the
vessels in the viscera and skin.
• Epinephrine (epi), also from the adrenal medulla, plays
a minor role in causing vasoconstriction.
– Epi also increases the rate and strength with which
the myocardium contracts.
• Nicotine (in tobacco) stimulates sympathetic
ganglionic neurons thus increasing release of NE from
postganglionic fibers and increasing secretion of NE
and epi from the adrenal medulla
39
Short-Term Chemical Controls (con’t)
• Antidiuretic hormone (ADH or vasopressin) is
produced by the hypothalamus and released from the
neurohypophysis (see A&P I: Unit 11- Endocrine
System).
– Its main role is to stimulate water reabsorption,
which affects long-term control of BP.
– At high levels, ADH causes vasoconstriction
(hence, its alternate name - vasopressin).
40
Short-Term Chemical Controls (con’t)
• Angiotensin II (see A&P I: Unit 11 - Endocrine; this
pathway is covered in detail later under indirect renal
control)
– Renin secreted by the kidney acts on
angiotensinogen and converts it to angiotensin I.
This is converted to angiotensin II.
– Angiotensin II causes intense vasoconstriction
– Angiotensin II stimulates secretion of ADH and
aldosterone (long term control).
41
Short-Term Chemical Controls (con’t)
• Atrial natriuretic peptide (ANP) is secreted by the atria
of heart. ANP causes general vasodilation and
antagonizes aldosterone.
• Alcohol (ethanol) depresses the vasomotor center
leading to decreased vasomotor tone. (What does this
do to pressure?)
– Alcohol also inhibits ADH secretion, which affects
both short-term and long-term pressure.
• Inflammatory chemicals cause vasodilation.
– They include histamine, prostacyclins, kinins and
others.
– They are released during the inflammatory response.
42
Short-Term Chemical Controls (con’t)
• Endothelium-derived factors affect vascular smooth
muscle and cause either vasoconstriction or vasodilation.
– Endothelin is a potent vasoconstrictor, released in
response to low blood flow (according to Marieb;
NOTE: other authors’ work suggests that damage to
the endothelium by physical trauma or ischemia is
more important in causing release).
– Nitric oxide (NO) acts as a vasodilator and is
released in response to high blood flow (according
to Marieb). NO causes systemic and local
vasodilation.
43
Long-Term Control of Resistance:
Renal Regulation
• Long-term control is aimed at regulating blood volume
(BV).
• Blood volume important to: venous pressure, venous
return, EDV, SV, and CO (see Topic 2: Heart).
• Long-term control is accomplished via the kidneys as:
– direct renal control, and
– indirect renal control.
44
Direct Renal Control
• Direct renal control is due to the affect of pressure on
filtration. (Filtration will be covered with Topic 10 Urinary System.)
• Increased BP creates more pressure for filtration
resulting in increased filtration. The more fluid
filtered, the greater the increased water loss; the
greater the water loss, the lower the volume, which
leads to decreased BP.
• Decreased BP creates less pressure, which decreases
filtration, thus decreasing water loss leading to
increased BV and increased pressure.
Fig. 20.9, p. 735
45
Indirect Renal Control
• The kidneys exert indirect control through the reninangiotensin pathway.
• Renin is secreted in response to decreased blood
pressure and sympathetic impulses.
• Decreased BP (or symphatetic impulses) stimulates the
juxtaglomerular cells of the kidney tubules to secrete
renin.
– Renin starts an enzymatic cascade that converts
angiotensinogen to angiotensin I. Angiotensin I is
converted to angiotensin II (see short-term control).
Fig. 20.9, p. 735
46
Blood Pressure Disorders: Hypotension
Hypotension refers to a systemic systolic BP less than
100 mm Hg.
• Orthostatic hypotension occurs as a drop in BP on
rising from sitting or lying. It is common in the
elderly.
• Chronic hypotension is a long-term depression in BP.
– Possible causes include poor nutrition, Addison’s
disease, and hypothyroidism.
• Acute hypotension is a rapid drop in BP.
– Acute hypotension is most often due to
hemorrhage and is a sign of circulatory shock.
47
Blood Pressure Disorders: Hypertension
Hypertension is a long-term elevation of arterial pressure
greater than 140/90.
• Hypertension causes damage to the heart, kidneys,
brain (stroke), and blood vessels overall.
• Hypertension is referred to as Primary if no cause is
clearly identifed. It accounts for about 90% of all
cases.
• Hypertension is referred to as secondary if a cause is
clearly identified. It accounts for about 10% of cases.
48
BP Disorders: Primary Hypertension
• Possible causes of primary hypertension include:
– diets high in Na+, saturated fat, cholesterol;
– diets low in K+, Ca2+, Mg2+;
– obesity (which increases angiogenesis), heredity,
age (due to loss of elasticity);
– stress (due to increased vasomotor tone); and
– smoking (due to the effect of nicotine).
• Treatment is aimed at changes in diet, weight loss,
exercise, stress management.
– Antihypertensive drugs, such as diuretics (which
decrease blood volume), beta-blockers (see A&P I:
Unit IX - ANS), and calcium-channel blockers (See
Topic 2), may be used.
49
BP Disorders: Secondary Hypertension
• Identifiable causes leading to secondary hypertension
include:
– excess renin secretion;
– arteriosclerosis;
– hyperthyroidism; and
– Cushing’s disease.
• Treatment aimed at eliminating the cause.
50
Changes in Blood Distribution
During Exercise
• During exercise, skeletal muscle becomes more
active and requires much more oxygen for aerobic
ATP synthesis (see A&P I: Unit 13 - Muscle)
• Total flow increases from ~ 5,800 ml/min at rest to ~
17,500 ml/min during exercise due to changes in
cardiac output.
• Flow to the Brain remains relatively steady (~750
ml/min).
• Flow to skeletal muscle and the heart increases
dramatically to supply oxygen and nutrients and
remove wastes from these hard-working muscles.
Fig. 20.12, p. 738
51
Changes in Blood Distribution
During Exercise
• Flow to the skin increases for removal of heat
generated increased muscle activity (i.e., for
thermoregulation).
• Flow to the kidney decreases, which decreases urine
output and helps to conserve water and maintain
pressure.
• Flow to abdominal organs and most other structures
decreases as blood is redirected to skeletal muscle &
heart.
Fig. 20.12, p. 738
52
Tissue Perfusion
• Tissue perfusion refers to blood flow through tissues.
• Flow varies with the need of the tissue.
• Functions of tissue perfusion include:
1) delivery of oxygen & nutrients, removal of wastes
from most tissues;
2) gas exchange in the lung;
3) absorption of nutrients from gut; and
4) urine production in kidney.
Fig. 20.12, p. 738
53
Velocity of Blood Flow
• The velocity of blood flow is inversely related to the
total cross-sectional area of the blood vessels to be
filled.
• Branching of arteries, arterioles and capillaries
increases cross-sectional area.
• Velocity is lowest in capillaries due to their vast crosssectional area.
– This is important in that it allows time for exchange
between blood and tissues.
• Velocity increases as capillaries rejoin to form venules
and venules join to form veins.
Fig. 20.13, p. 739
54
Autoregulation of Blood Flow
• Autoregulation refers to the local (intrinsic) regulation
of blood flow.
– Blood vessels serving tissues adjust to meet needs
of tissue by dilating or constricting.
– If blood flow is inadequate, tissue metabolism
decreases and cells may die.
55
Autoregulation of Blood Flow
• Long-term autoregulation refers to an increase in
number and size of blood vessels. This is called
angiogenesis.
• Short-term autoregulation occurs by mechanisms of
control:
– Metabolic control is a response to chemical needs of
tissue.
– Myogenic control is a response to stretch of the
vessel.
56
Metabolic Control of Blood Flow
• Metabolic control maintains the proper chemical
environment for cells.
• Metabolic control causes relaxation (vasodilation) of
the precapillary sphincter to increase blood flow to
active tissues.
– Active hyperemia occurs due to chemical changes
associated with hard-working tissues:
° decreased oxygen and/or other nutrients; and
° products of metabolic activity such as increased
K+, adenosine, lactic acid, and H+ (decreased
pH).
57
Metabolic Control (con’t)
• Other important vasodilating chemicals include:
– nitric oxide (NO), which attaches to hemoglobin in
lungs as O2 is loaded; NO is released at capillaries
as O2 is released; and
– inflammatory chemicals (histamine, kinins) released
in response to the inflammatory response (see Topic
6 - Resistance).
58
Myogenic Control of Blood Flow
• Myogenic control maintains relatively steady flow to
tissues in spite of changes in overall BP.
• Myogenic control is based on the response of vascular
smooth muscle to stretch.
– Increased stretch (due to increased pressure or flow)
leads to contraction, which is seen as
vasoconstriction. This decreases flow.
– Decreased stretch (due to decreased pressure of
flow) leads to relaxation, which is seen as
vasodilation. This increases flow.
59
Myogenic Control of Blood Flow
• Reactive hyperemia refers to a dramatic increase in
blood flow following removal of blockage
– This results from:
° stretching of arteriole upstream from blockage
due to accumulation of blood, and
° accumulation of wastes in the tissue.
60
Capillary Dynamics
Movement across the capillary wall is based on
gradients. Three important gradients are:
• Solute gradients, which lead to diffusion;
• Water (osmotic) gradients, which promote
osmosis; and
• Pressure gradients (hydrostatic pressure), which
force fluid and solutes across the membrane.
Fig. 20.14, p. 742
61
Diffusion
• Small, water-soluble molecules pass through small
intercellular clefts between endothelial cells
(desmosomes are loose cell junctions).
• Lipids and lipid-soluble (non-polar) materials diffuse
directly through the lipid bilayer of the endothelial
cells.
• Osmosis is a special form of diffusion in which the
solvent (i.e., water) moves across the membrane.
(Osmosis is the diffusion of water.)
– Water moves toward the area with the lower water
(higher solute) concentration.
62
Bulk Fluid Flow
Moves fluids and dissolved substances through capillary
walls together using the following forces:
• Hydrostatic Pressure:
– which is the physical pressure exerted by a fluid in
an enclosed space.
– Fluids and dissolved substances move from areas
of high to areas of low hydrostatic pressure.
• Osmotic Pressure:
– which is the “pull” exerted on the solvent by
solutes in solution.
– The more solute in a solution, the greater its
osmotic pressure.
63
Forces Moving Fluid OUT Of Capillary
Forces that move fluid OUT of the capillary move fluid
INTO the interstitial space.
• Capillary hydrostatic pressure (HPc) is also called
capillary blood pressure (or blood hydrostatic
pressure) and is the physical pressure of the fluid in
the capillary.
– HPc pushes fluid out of the capillary.
– The average HPc at the arterial end of the capillary
is 35 mm Hg.
– The average HPc at the venous end of the capillary
is 17 mm Hg.
64
Forces Moving Fluid OUT Of Capillary
• Interstitial fluid osmotic pressure (OPif ) is created
mainly by proteins in interstitial fluid that exert
osmotic pressure on plasma.
– OPif pulls fluid out of capillary into tissues.
– BUT, normally very little protein is present in the
IF; the average value is 1 mm Hg, which is what is
used in equations.
65
Forces Moving Fluid INTO Capillary
Forces that move fluid INTO the capillary move fluid
OUT of the interstitial space.
• Interstitial fluid hydrostatic pressure (HPif) is the
physical pressure pushing interstitial fluid into the
capillary.
– HPif ranges from slightly negative to slightly
positive because fluid is normally removed by the
lymphatic system.
– 0 mm Hg is generally used in equations.
66
Forces Moving Fluid INTO Capillary
• Capillary osmotic pressure (OPc) is the pressure due to
the presence of large, nondiffusible molecules (e.g.,
plasma proteins) that draw fluid into the capillary from
the interstitial fluid.
– The average value of OPc is 26 mm Hg
– Little change occurs along the capillary from the
arterial end to the venous end.
67
Net Filtration Pressure
• Net filtration pressure (NFP) is the sum of all
hydrostatic and osmotic forces acting on fluids as they
move through capillary walls.
• NFP can be seen as difference between forces moving
fluid out of the capillary and forces moving fluid into it
net filtration pressure (NFP) =
[sum of outward forces] – [sum of inward forces]
= [HPc + OPif]
- [HPif + OPc]
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Net Filtration Pressure
• At the arterial end:
Forces out are HPc (= 35mm Hg); and OPif (= 1 mm Hg)
Forces in are HPif (= 0 mm Hg); and OPc (= 26 mm Hg)
NFP = [35mm Hg + 1 mm Hg] – [0 mm Hg + 26 mm Hg]
= 10 mm Hg (flow OUT OF capillary at arterial end)
HPc
+
35 mm Hg
Hpif
0 mm Hg
OPif
= 36 mm Hg OUT
1 mm Hg
+
OPc
= 26 mm Hg IN
26 mm Hg
NFP = (OUT-IN) = 10 mm Hg OUT
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Net Filtration Pressure
• At the venous end:
Forces out are HPc (= 17 mm Hg); and OPif (= 1 mm Hg);
Forces in are HPif (= 0 mm Hg); and OPc (= 26 mm Hg)
NFP = [17 mm Hg + 1 mm Hg] – [26 mm Hg + 0 mm Hg]
= - 8 mm Hg (net flow INTO capillary at venous end)
18 mm Hg OUT = OPif
+
1 mm Hg
26 mm Hg IN = OPc
26 mm Hg
HPc
17 mm Hg
+
Hpif
0 mm Hg
NFP = (OUT- IN) = -8 mm Hg (IN)
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Net Filtration Pressure
• NFP results in a net LOSS of fluid from capillary to
interstitial fluid:
10 mm Hg loss from capillary at the arterial end
- 8 mm Hg gain to capillary at the venous end
2 mm Hg net LOSS along the length of the capillary
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Net Filtration Pressure
• NFP can also be seen as difference in hydrostatic
pressures minus difference in osmotic pressures
= (HPc – HPif) - (OPc – OPif)
• The difference in hydrostatic pressures is the Net
Hydrostatic Pressure.
NHP = HPc – HPif; HPif is generally 0 mm Hg.
– at the arterial end, NHP is:
35mm Hg – 0 mm Hg = 35mm Hg
– at the venous end, NHP is:
17mm Hg – 0mm Hg = 17mm Hg
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Net Filtration Pressure
• The difference in osmotic pressures is the Net Osmotic
Pressure.
• NOP = OPc – OPif
= 26 mm Hg – 1 mm Hg = 25 mm Hg
• This normally does not change along length of
capillary.
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Net Filtration Pressure
At the arterial end
NFP = net hydrostatic presssure – net osmotic pressure
= [35mm Hg – 0mm Hg] – [26mm Hg – 1mm Hg]
= 35mm Hg
–
25mm Hg
= 10 mm Hg (fluid moves out of the capillary)
See also Fig. 20.15, p. 743
HPc
OPif
35 mm Hg
1 mm Hg
Hpif
OPc
0 mm Hg
26 mm Hg
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Net Filtration Pressure
At venous end
NFP = net hydrostatic presssure – net osmotic pressure
= [17 mm Hg – 0 mm Hg] – [26mm Hg – 1mm Hg]
= - 8 mm Hg (fluid moves into capillary)
See also Fig. 20.15, p. 743
OPif
HPc
1 mm Hg
17 mm Hg
OPc
Hpif
26 mm Hg
0 mm Hg
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Edema
• Edema refers to abnormal accumulation of fluid in
tissues.
• Each of the following contributes to edema (try to figure
out why):
– increased MAP;
– venous obstruction;
– leakage of plasma protein across into interstitial fluid
as a result of an allergic reaction;
– myxedema, which is an accumulation of glycoprotin
in the interstitial fluid as a result of hypothyroidism;
– decreased plasma protein production, due to protein
malnutrition (kwashiorkor); and
– destruction of lymphatic drainage channels as in
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filariasis (blockage of lymphatics by parasitic worms).
Circulatory Shock
• Circulatory shock refers to “any condition in which
blood vessels are inadequately filled and blood cannot
circulate normally” (i.e., it decreases tissue perfusion).
• Shock results in decreased flow to tissues leading to
cell death (necrosis).
• Signs of shock include:
– rapid, but weak, heart beat (“thready” pulse);
– intense vasoconstriction; and
– a sharp drop in blood pressure;
• Treatment depends on the cause.
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Cardiogenic Shock
• In cardiogenic shock the heart is not able to pump
enough blood.
– This is often due to myocardial damage (multiple
infarcts).
– Cardiogenic shock is the leading cause of death due
to shock, although it is not the most common type of
shock.
– Treatment is aimed at promoting heart function by
encouraging a stronger heart beat (positive inotropic
agents - see Topic 2) and vasoconstriction to
increase pressure.
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Hypovolemic Shock
• Hypovolemic shock occurs when there is large scale
loss of fluid.
– This is the most common type of shock.
– Causes include:
° acute hemorrhage (hemorrhagic shock);
° severe vomiting or diarrhea; and
° extensive burns (especially third-degree burns;
see A&P I - Unit II: The Integumentary System)
– Treatment is aimed at restoring fluids as rapidly as
possible.
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Types of Circulatory Shock
• Vascular shock occurs when there is extreme
vasodilation resulting in decreased peripheral
resistance. Treatment is aimed at vasoconstriction.
– Anaphylaxis (anaphylactic shock) is a systemic
reaction to allergen (e.g., bee sting) introduced into
the blood. Antihistamines may be administered.
– Neurogenic shock occurs when vasomotor tone is
lost due to altered ANS (sympathetic) function.
Some types of medications and spinal anesthesia can
alter sympathetic outflow.
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Types of Circulatory Shock
– Septic shock results from a systemic reaction to
bacteria or their toxins. This is the second most
deadly form of shock. Treatment includes antibiotics
in addition to vasoconstrictors.
– Prolonged exposure to heat (e.g., sunbathing) can
cause a transient state of shock due to excessive
vasodilation of cutaneous vessels. Cooling the body
will generally eliminate the symptoms.
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