I. Characteristics of Blood Vessels
A. Arteries
1. Thick-walled, muscular, elastic
2. Rapid blood flow
3. Withstand high pressure
4. Sympathetic innervation
B. Arterioles
1. Muscular wall (smooth muscle) which can be regulated
by ANS
2. Control point for tissue perfusion
3. Sympathetic innervation
C. Capillaries
1. Single cell layer thick to allow for exchange
2. Not innervated
D. Venules & Veins
1. Form reservoir of blood which is affected by needs
of body
2. Thin-walled
3. Sympathetic innervation
II. Factors Affecting Blood Flow
A. Summary
Flow=Pressure gradient / resistance
B. Pressure Differential
Pressure gradient
Arterial pressure is higher at the heart than at the capillary
C. Resistance
1. Factors affecting resistance are:
R= viscosity x length
r4
a. viscosity of fluid (blood)
b. Length of blood vessels
c. Radius of blood vessels
2. Viscosity of blood
a. increased viscosity increases resistance
b. Viscosity is affected by hematocrit
3. Length of vessels
a. Effect of increased BW on vessel length
4. Radius of vessels
a. Changes rapidly
b. Increased radius decreases resistance
c. ANS control
-sympathetic innervation causes vasoconstriction
d. Local changes
-Tissue metabolism
increased need for oxygen leads to vasodilation
either by production of a vasodilator substance or by direct effect of
oxygen on precapillary sphincters
e.g. reactive hyperemia (restriction of blood
flow and depriving muscle of nutrients leads to increased perfusion later
e.g. active hyperemia when muscle is exercising
or gland is secreting etc.
-EDRF , endothelial derived relaxing factor or
NO (nitrous oxide)
e. Hormones
1) Angiotensin II a potent vasoconstrictor
2) Vasopressin (aka ADH) (also a vasoconstrictor)
3) Both of above also affect blood volume by influencing
the kidney
4) Endothelin
a vasoconstricting hormone located in cells
of endothelium. Damage to blood vessels causes release of endothelin.
5) Inflammatory hormones (vasodilators)
-bradykinin & prostaglandins are released
during injury
-histamine released during allergic response
or injury
f. Temperature
1) heat--vasodilation
2) cold-vasoconstriction
D. Effect of the venous pump
1. Valves in veins are 1-way which open and close in response
to pressure
2. Muscles squeeze blood forward
3. Standing still, blood pools in feet
4. Can get edema as increased pressure in lower limbs
forces fluid out of capillaries into interstitial spaces
E. Example of changes in blood flow/cardiac output due
to exercise
1. Changes in ANS.
2. Activation of sympathetic nervous system.
a. Effect on heart rate.
b. Effect on venous return.
-vasoconstriction of veins
c. Effect on contractility of heart
3. Muscular effects
-lungs and muscle squeezing
4. Decreased resistance as increase blood flow to exercising
muscle
III. Blood Pressure (Arterial pressure)
A. Summary of two main factors affecting arterial pressure
1. Cardiac output
2. TPR (total peripheral resistance)
3. MAP ªC.O. x TPR
B. What is TPR?
The sum of resistance to flow in all of peripheral circulation.
C. Maintenance of Blood pressure
1. Homeostasis is critical
a. Hypotension-inadequate perfusion, esp of brain
b. Hypertension-strain on heart and damage to vessels
2. Sympathetic tone
a. Usually always a degree of sympathetic tone
b. Vasomotor nerves leave spinal cord through all
thoracic and 1st and 2nd lumbar regions
c. Spinal anesthesia
-total anesthesia blocks transmission of not
only pain impulses but also sympathetic impulses maintaining vascular tone,
leading to a rapid decrease in arterial pressure
3. Baroreceptor reflex arc (nervous system control of
arterial pressure)
a. Baroreceptors
-located in walls of carotid sinus and aortic arch
-sense stretch so that increased BP leads to
increased stretch and increased firing of afferent neurons
b. Project into medulla of brain stem
c. Increased firing rate of afferent baroreceptor
neurons leads to inhibition of vasoconstricter center and excitement of
vagal center
d. Results in :
Decreased HR
Decreased SV
Decreased CO
Decreased resistance
e. Effects of postural changes
-rapid standing from prone position
(see fig. 18-8)
4. Chemoreceptors (more detail in respiration)
a. Located in carotid and aortic bodies
b. Sense decreased oxygen, increased carbon dioxide
and decreased pH as blood flows past.
c. Decreased blood flow results in decreased removal
of CO2 and H ions and decreased oxygen delivery to chemosensitive cells.
5. Hormonal control
a. ANP (atrial natriuretic peptide)
-atrial stretch results in release of ANP
-ANP acts on kidneys to decrease sodium reabsorption
and also affects renal blood flow
-therefore more water is lost to urine resulting
in lowering BP
b. ADH
-baroreceptors in hypothalamus sense large decreases
in blood pressure (such as in hemorrhage)
-release of ADH and water retention
c. Angio II
-we’ll discuss Angio II during kidney, but increases
BP by increasing fluid retention and vasoconstrictive effects
d. Low pressure receptors in pulmonary circulation
e. CNS ischemic response
-cerebral ischemia due to low BP (hemorrhage) leads
to activation of sympathetic and inactivation of PS
- a last-ditch effort to save CNS perfusion
-only kicks in at very low BP’s
D. Hypertension
1. Lethal effects due to:
a. excess work load on heart (CHF more likely as left
side hypertrophy ensues and blood backs up into pulmonary circulation)
b. rupture of cerebral vessles (stroke)
c. kidney hemorrhage
2. Essential hypertension or primary
a. unknown origin, but some hereditary tendency
b. increased MAP
c. decreased renal blood flow (increased resistance
to flow through kidneys)
d. kidneys don’t excrete salt and water normally
(leading to increased blood volume) unless at high arterial pressures
e. Treatment
- drugs to increase renal blood flow
- diuretics to decrease ECF volume
3. Preeclampsia/pregnancy induced hypertension
a. increased blood volume
b. increased salt and water retention by kidneys
4. Atherosclerosis
a. increased TPR due to decreased vessel radius
5. Endocrine disorders
a. ADH, aldosterone, renin-angiotensin system
E. Hypotension
1. Dehydration
2. orthostatic hypotension